Microbio Test 3

Describe the steps of antigen processing from the receptor-mediated method.

1. Antigen presentation and binding by CD4+ T cell occurs. 2. The activated CD4+ T cell secretes interleukin-2 (IL-2) and expresses its receptor IL-2R for autostimulation. 3. Clonal expansion and differentiation produces a population of memory and effector T(h) cells.

Describe the steps of phagocytosis.

1. Opsonized microbe binds to phagocyte surface receptors. 2. Cytoplasmic extensions surround and engulf the bound microbe. 3. Phagosome forms and acidification begins. 4. The phagosome fuses with lysosome to form a phagolysosome. 5. Oxidative burst and lysosomal enzymes kill the microbe. 6. Exocytosis expels the debris!

What are 3 reasons why normal flora is important? What are some normal flora characteristics?

1. Supply of certain vitamins (K, B12, folate, biotin) 2. Keeps immune system "revved up" 3. Ecological stability = excludes potential pathogens Characteristics: very complex with more than 200 species of bacteria; make up depends on factors from host like genetics, age, sex, stress, nutrition, diet, etc Normal flora of humans consists of a few eukaryotic fungi and protists, some eukarya, but mainly bacteria

What are the 5 main components needed for adaptive immunity?

A B cell has a BCR attached to its surface. An antibody attached to an antigen binds to the BCR. Each antigen has multiple epitopes that antibodies can bind to.

What is a carbuncle? What is pus?

A carbuncle is more than 1 small abscess coming together to form a larger one. Pus is the body's result of the inflammatory response. It works to fight an infection.

What is adaptive immunity?

Adaptive immunity is only found in jawed organisms or higher vertebrates. If an innate, unspecific immunity response isn't clear enough to an infection, adaptive immunity can assist. This system is HIGHLY specific for individual foreign molecules or pathogens. It has the ability to "Remember" previous exposures, providing long-term protection against re-exposure to the same pathogens.

What cells can be opsonized? What happens post-opsonization?

Gram positive, gram negative, and viruses can all be opsonized. As long as there is an antibody that will bind to it or the protein C3b to bind to it, it can be opsonized. After opsonization, phagocytosis takes place.

What are the oxygen products of the respiratory burst involved in killing infectious cells?

H2O2, HOCl, OH, O2, NO

What are the consequences of systemic inflammation?

If inflammation gets out of hand, it can be damaging. This might happen if microbes or their products get into the bloodstream. The whole body is affected by systemic inflammation. Septicemia = bacteria enters the blood steam and is able to reach the organs which it usually can't get to Septic shock = widespread presence of bacteria in the body induces system-wide inflammation; mostly caused by gram-negative bacteria, but can be caused by gram + and fungi. Toxic Shock = overstimulation of immune responses by bacterial exotoxins in the blood; There is a bacterium somewhere that's making enough of a particular toxin that it can spread out and overwhelm the immune system. Death rates of 30-50% aren't uncommon with septic or toxic shock. 1L-1 and TNF-alpha cytokines are potent mediators of systemic inflammation induced by microbes or their products.

Describe how B cells serve as antigen presenting cells.

If you are a B cell, your B cell receptor is a membrane bound antibody, the same antibody that the B cell will eventually secrete. One antibody binds to one particular epitope. The antibody gets endocytosed, then presented as an antigen. It's an antigen-presenting cell so it presents the antigen on MHC class 2. It now has a peptide of that antigen that it evolved to detect. That's the only epitope that that B cell has to detect an antigen.

How long does it take for IPG to form if you've never been infected before? What solution do we have for this in today's world?

If you have a primary response and you've never been infected before, it takes you about 2 weeks to make IPG. In today's world, this is why we vaccinate in order for exposure to antigen to not basically shock your body and force it to wait to fight the infection.

Describe what happens to extracelllular and intracellular bacteria or antigen.

If you have an extracellular bacteria or another antigen like a toxin, you have an antigen-presenting cell that brings it in. it can bind that to MHC class II. CD4+ T cells work with MHC class 2. The CD4+ T helper cell will see the antigen and if it binds to the antigen, the TCR (T cell receptor) will need to see MHC and a peptide. In this case, since the helper cell is CD4+, it must see MHC class 2, specifically. If the antigen is endogenous, an intracellular virus or bacterium, it will need to work with MHC class 1. They will bind to cytotoxic T cells, which are CD8+ T cells.

Define immunogen antigen, epitope, and antibody.

Immunogen: any material capable of eliciting an immune response (a robust antibody or T-cell response) Antigen: molecule recognized by immune response, by a specific antibody or TCR of T-cell. It is seen as nonself. Epitope: molecular structure recognized by the immune response. It's an antigenic determinant that interacts with a single antibody molecule. Complex antigens might have many possible epitopes. Epitopes can be linear, formed by a specific sequence of amino acids or sugars, or they can be conformational, formed by 3 dimensional structure. Antibody: an immunoglobulin molecule (protein) that interacts with an antigen; produced by B cells

What is immunology?

Immunology is the study of the components and processes of the immune system, which distinguishes foreign substances from self structures. Vertebrates have 2 systems: The innate, non-specific system and the adaptive, specific system. Together, these defend the body against foreign agents and cancerous cells.

Define disease, infectious disease, zoonotic disease, and pathogens.

disease: a disturbance in normal functioning of an organism Infectious disease: caused by a mcirobe and can be transmitted from host to host (EX: influezna, HIV, hepatitis B) Zoonotic Diseases: infectious disease of animals that can cause disease when transmitted to humans (EX: rabies, West Nile fever) Pathogens = microbes which are frequently associated with disease production

What was the breakthrough that changed human life expectancy?

introduction of antibiotics

What are the 3 antigen presenting cells?

macrophages, dendritic ells, B cells

Describe the Barrel-stave model.

...

Explain the process of creating and the function of a cytotoxic effector T cel.

1. A naive T cell is activated by an APC (antigen presenting cell). 2. Clonal expansion occurs producing a population of effector and memory T cells. 3. Effector T cells migrate ot the site of infection and bind to infecte cells. 4. Binding causes activation of the effector function, such as cytotoxic killing of the infected cell. 5. A late encounter occurs between a memory T cell and an APC presenting the same antigen. 6. Activation and clonal expansion of the memory T cell into effector and memory T cells occurs.

What are the 6 mechanisms of innate immunity?

1. Anatomic Barriers: skin, mucous membrane, mucous 2. Chemical Barriers and Physiological Variables: bile, pH, temperature, iron-binding proteins 3. Clearance Mechanisms: phagocytosis 4. Enzymatic Proteins: lysozyme, complement 5. Chemical Defenses: superoxide, nitric oxide 6. Antimicrobial peptides: Defensins

Describe antigen processing involving CD8+ T cell.

1. Antigen presentation and binding by CD8+ T cell occurs. 2. The activated CD8+ T cell expresses interleukiin-2 receptor (IL-2R) that binds IL-2 produced from T(h) cells (which came from CD4+ antigen processing, remember). 3. Clonal expansion and differentiation produces a population of memory and effector T(c) cells (cytotoxic, killer cells). 4. The Tc effector cell binds to an infected target cell, causing degranulation. 5. The target cell undergoes apoptosis. 6. The cell fragments and microbes will be degraded by phagocytes.

What does activation of T cells require and what is the result of this activation?

1. Antigen presenting 2. Cell signaling 3. Production of stimulatory molecules. T-cell activation requires binding of the TCR with the specific peptide presented on major histocompatibility (MHC) molecules of Antigen Presenting cells (APCs). APCs include dendritic cells, macrophages, and B cells. While B cells have receptors on their surface and don't have to be presented, T-cells have to have a "wing man" to present them, an MHC molecule. As a result of activation, activated T cells expand and differentiate into either effector cells or memory cells.

What are the obligatory steps for infectious microorganisms?

1. Attachment +/- entry into body. This causes infection and requires that the pathogen evades the hosts' natural protective and cleaning mechanisms. 2. Local or general spread in the body-This is a local event in which spreading occurs. It requires that the microorganism can evade immediate local defenses, and the natural barriers in order to spread. 3. Multiplication-The microorganism multiplies. Many offspring will end up dying in the host or "en route" to a fresh host during this multiplication process. 4. Evasion of host defenses-This is the microbial answer to host defenses. The microorganism must evade phagocytic and immune defenses long enough for a full cycle within in the host to be completed. 5. Shedding (exit) from body-This is the transmission step. The microorganism must leave the body as a site and on a scale that ensures adequate spreading to the next, fresh host. EX: coughing, pooping 6. Cause damage in host-This is the pathology, disease step. It is not strictly necessary, but often occurs.

What are the 10 steps to the inflammatory response?

1. Bacteria enters tissue through a cut. 2. Vasodilator molecules are released like histamine. 3. Bacteria multiply and invade tissue. 4. Vasodilators concentration increase. 5. The blood vessel dilates, allowing more blood into the area. An increase in local temperature and redness occurs. 6. Vessel walls become more permeable. Fluid moves into the tissue, causing swelling. Extravasation of cells and molecules occurs. 7. Antibody and complement factors bind the bacteria. 8. Phagocytes engulf and destroy the bacteria. Cytokines are released, attracting more leukocytes. 9. Adhesion molecules are expressed on vessel walls to facilitate extravasation of immune cells. 10. Clotting is initiated to restrict access of bacteria to circulatory system.

Explain what happens to C3a and C5a when these complement proteins are released.

1. C3a and C5a stimulate mast cells to release their granules (vasoactie substances). This increases the permeability of blood vessels and facilitates the movement of phagocytes from the bloodstream. 2. C5a and C3a signal phagocytess to leave the bloodstream. PMNs and/or monocytes "home" to a gradient of C5a to find the locus of infection. 3. C3b binds to the surface of invading bacterium and makes it easier for phagocytes to ingest in a process called opsonization.

What are the two different types of adaptive immunity and what do these types entail? What are the advantages of adaptive immunity?

1. Humoral: actiivation of B cells; production of antibody 2. Cell Mediated: activation of T cells; generation of cytokines The advantages of adaptive immunity is that immune receptors and antigens are employed. Immune receptors bind to the antigen. T cells possess the T-cell receptors (TRCs). B cells possess immunoglobulin molecules, which are B-cell receptors (BCRs) when on the surface of a cell. Antibody is the secreted for of the BCR.

What are the two types of adaptive immunity and what are 2 examples of each?

1. Humoral: activation of B cells, production of antibody 2. Cell Mediated: activation of T cells, Generation of Cytokines

What are the 4 distinguishable types of microbial infection?

1. Microbial Attachment/Penetration Mechanism- 2. Biting arthropod- 3. Skin wound/animal bite- skin barrier must be broken In types 1-3, the antimicrobial defenses are still intact. 4. Antimicrobial defenses impaired: this is the type used with opportunistic organisms

Describe the steps or elements of host protective responses.

1. Microbial attack on human body. 2. Barriers, like the skin, are compromised. 3. Quick host response (innate responses like phagocytosis and complement) 4. Sound the alarm! (complement, chemokines) 5. Directed Attack (adaptive response, T-cells)

What is a synapse?

A synapse is an event in which a B cell and a T cell are working together in the world of immunology to get a very large response which ends up producing memory B cells and effector plasma B cells. It takes place because the T cell and the B cell see the same antigen!

Which cells have MHC class I and which have MHC class II. Why?

All cells but red blood cells have MHC class I, but only major antigen presenting cells have MHC class 2 because of the dark side of the immune response. If everyone presented an antigen all the time, eventually we'd be screwed! The immune system would basically overwhelm us and we could go into septic shock then die. The idea is that you need enough of an infection going on that an antigen presenting cell sees the antigen and activates those T cells. But you don't want too many T cells activated.

What is an allergy?

Allergies take place due to hypersensitivity when mast cells are degranulating too much in response to an allergen.

Besides MAC formation, what is another function of a complement protein?

Another function of a complement is opsonization/phagocytosis. Coating with the activated complement increases the chances of phagocytosis.

What is the difference between antimicrobial and antibiotics?

Antibiotics are man made while antimicrobials are naturally occuring.

What come from the lymphocytes and lymphoid tissues of the adaptive immunity system? What happens if proper differentiation of these cells doesn't happen?

B and T cells come from them. They originate in bone marrow and differentiate from there. You're making millions of these B and T cells, so the first thing that you want to do to dis-group the population is to get rid of all of the ones that would recognize you. T cells travel to the thymus to do this in an immature stage for further development. B cells go to the "bersa". Bone marrow and thymus are both generative lyphoid organs. Sometimes, proper differentiation doesn't take place and you can't get rid of the B and T cells that are "self". This is how auto-immune deficiencies develoop. You aren't born with the immune system of your parents. T and B cells are different and change as you develop, so your body must try and get rid of the bad, self-recognizing ones.

Where do B and T cells move to? What does this have to do with cancer patients? What is the whole idea of the lymphoid system?

B and T cells move to the primary lymphoid tissue sites. Then they have to migrate to secondary sties. Lymphoid tissue is FULL of T and B cells. This is why people with cancer always have their lymphoid tissues checked. The whole idea of the lymphoid system is to make cells, teach them what to see and recognize, then get them to where they need to go in order to fight an infection.

Describe the antigen-presenting cells called B cells.

B cells are critical for adaptive immunity because they produce antibodies. They present MHC II:peptide complexes to CD4+ T cells. B-cell receptors (BCRs) trap the foreign antigen. The antigen is broken down into fragments after being ingested. These fragments are loaded onto MHC class II molecules and presented to CD4+ T cells, inducing them to secrete cytokines. The cytokines help the B cell to differentiate into an antibody-secreting plasma cell and/or a memory B cell. Most B cells need the help of T-cell cytokines to become fully activated-and they cannot do this without help from presenting antigens.

What is extravasation?

Capillaries, made out of endothelial cells, allow for expansion and have holes in their walls that allow for things to come into them. This is called extravasation. When you have an inflammatory response, there are receptors that make bacteria stop at those points, not allowing the bacterial cells to go through the holes through extravasation. As time goes on, expansion and pulling apart takes place to allow other things to come across the capillary walls. Extravasation also is the process by which disease-fighting cells can travel across the wall of the blood vessel and get to the site of infection.

Describe the cell mediated immune response, the second type of adaptive immunity.

Cell-mediated immunity involves activation of T lymphocytes and other cells capable of cytotoxic activity against foreign agents.

What is the difference between colonization, infection, and disease?

Colonization happens when the organism doesn't interfere with the normal physiology of the host. The microbe has established itself and is multiplying on/in the host, but normal physiology isn't altered. Infection is when the microbe has a parasitic relationship with the host. Disease is the presence of an organism which leads to damage of the human host. Damage may arise from the invading organism (a toxin) or from the host immune response to the organism.

Define communicable disease, infection dose, incubation period, types of duration, and convalescence.

Communicable diseases are contagious and are spread easily from one host to another. Infection dose is the number of microbes required to establish an infection. Incubation period is the interval of time between introduction/exposure of an organism to host and the onset of illness. Duration can be one of 3 types: Acute is a rapid onset of symptoms. Chronic is an infection that develops slowly and lasts longer. Latent is an infection that is never completely eliminated. Convalescence is the period of recuperation and recovery after illness. The infectious agent, however, may still be spread. So in summary, a communicable disease is contagious, has a specific infectious dose which tells us how many microbes are needed to establish infection, and an incubation period, the time between when the microbe is introduced to a host and when infection kicks in. Once the infection has taken its domain, its duration can be acute, chronic or latent and a period of convalescence will take place after the infection has passed.

Describe the antigen-presenting cells called dendritic cells.

Dendritic cells are very efficient at antigen uptake, but not efficient killers of microbes. They are named for their many long cytoplasmic extensions that resemble nerve cell dendrites. They are formed in bone marrow but live in maturity in various tissues.

Describe TLR specificity in terms of binding and responding.

Different TLRs (toll-like receptors) can detect different PAMPS. TLR4 binds LPS. TLR9 recognizes unmethylated CpG dinucleotides. TLR3 detects double-stranded RNA (common to viruses). Different TLRs may produce different cytokine responses for MAXIMUM effectiveness. Proinflammatory cytokines have the job of telling your body that you ahve an infection and that the inflammatory response is needed to clear that infection. For example, TLR4 binding of LPS stimulates the production of IL-1 and TNF-alpha. These cytokines initiate a strong antibacterial response.

What takes place during development of adaptive immunity? When are receptors formed?

During development, gene arrangements produce a very large number of unique TCRs and BCRs. This increases the chances of reaction against pathogens. Receptors are formed BEFORE exposure to pathogens.

What takes place during opsonization by phagocytes?

During opsonization, the microbial surface is coated with an effector protein that promotes phagocytosis. The phagocytic cell has different receptors to promote opsonization. All phagocytes have Fc receptors that allow it to attach to the antibodies that bind during the coating process of opsonization.

Describe effector T cells and their functions.

Effector T cells are the ACTION cells. They are short lived and armed with direct immune functions. In T cells, effector form depends on co-receptors. CD4+ T cells cause for the secretion of large amounts of cytokine to enhance and direct actions of other immune cells. These are helper T cells who secrete cytokines, the "alarms" that allow for talking and communicating between cells. They help your body to know what to do to keep itself from dying. CD8+ cells cause for the cytotoxic killing of infected cells by the release of granzymes/perforin near the contacted target cell, initiating apoptosis. CD8+ T cellls is a cytotoxic cell that must bind to a specific antigen. CD8+ T cells are similar to natural killer cells.

What is the difference between effector cells and memory cells?

Effector cells are short-lived and actively fight infection through the recognition of antigen. Memory cells persist in the body for rapid response to subsequent, secondary antigen.

How do new infectious diseases arise? Why were we previously misconceived?

Emerging or re-emerging infectious diseases may arise by encountering a new population. An old pathogen might develop antibiotic resistance, allowing it to promote a new disease. An example is the transfer of simian immunodeficiency virus (SIV) into humans as HIV. Another is Lyme disease. Before, we thought that all diseases on earth were present at the beginning. we never thought of diseases as being able to emerge.

What are the "cytotoxic" cells? What is their purpose? What is the problem with them?

Eosionophils, basophils and mast cells Since some pathogens like extracellular parastic worms and certain fungi are too big to be killed by phagocytosis, they must be killed another way. Cytotoxic cells help fight such pathogens by releasing toxic granule contents near them and killing them through a degranulation process. The prolem with their degranulation killing process is that a giant explosion results from it, which releases all of the bad contents into the cellular environment and could cause other nearby cells to be infected.

How can T cells be so specific?

Even though TONS of T cells are produced, they mature in thymus and are screened to avoid excessive self-reactivity. "Good" T cells with anti-foreign molecule TCRs are released to the peripheral bloodstream. Additionally, co-receptors, either CD4 or CD8, must also correctly interact with the MHC molecule. CD4 interacts with MHC class I while CD8 interacts with MHC class II. These specific requirements help provide the correct activation signal to the correct type of T cell.

What problem have we run into with antibiotic resistance?

Every time we found resistance, we simply made a new antibiotic. In a sense, we developed a mindset of being invincible. Now, we're running out of effective antibiotics! It takes 30 years to make a new antibiotic. There are emerging and re-emerging infectious diseases. We underestimated the ability of the microorganisms to efficiently and quickly change their genetic makeup to take advantage of new opportunities to infect. We also didn't take into account the impact of changing human practices. So now, we're at a standoff. We have to stay on top of the problem of antibiotic resistance and keep working on this issue.

What are the types of infections in regards to where they arise?

Exogenous infections are diseases which arise from exposure to an external source. For example, diseases caused by influenza virus. Endogenous infections, which are more common, are diseases arising from host microbial flora. Examples are E. coli and staphylococcus aureus.

Describe the time line of exposure to antigen.

Exposure to a new infectious agent produces a primary immune response which can take 7-14 days to peak, producing memory lymphocytes as a result and clearing the pathogen. Subsequent exposure results in a memory or anamnestic response, a secondary immune response which is much faster and more potent than the primary. If the primary took 14 days to peak, the secondary response would peak at 5 days.and stay relatively active, meaning there wouldn't be a huge drop off.

Describe the steps involved in extracellular bacteria/exogenous antigen pathways versus intracellular bacteria and viruses/endogenous antigen pathways.

Extracellular Bacteria/Exogenous Antigens: 1. Extracellular bacteria is ingested and killed by a macrophage. 2. Bacterial peptides are presented in complex with MHC class II. 3. Peptide-MHC II complex stimulates T-helper cells (CD4+). 4. T-helper cells (Th2) produce various cytokines to direct a robust immmune response including stimulating B cells to produce antibodies. Intracellular Bacteria and viruses/Endogenous Antigens: 1. Intracellulaar bacteria enter cytoplasm of macrophage. 2. Bacterial peptides presented in complex with MHC-1. 3. Peptide-MHC-1 complex stimulates Cytotoxic cells (CD8+). 4. Activated cytotoxic T cells kill any host cells displaying the bacterial peptide-MHC I complex that activated them.

How are infectious diseases transmitted?

First off, transmission is the spread of an infectious agent from one host to another. It may also occur from a pathogen's natural source, a reservoir, to a host. There are several routes of transmission. 1. Contact can be direct--a physical contact between infected organism and susceptible host, or it can be indirect-an object carries the agent between infected and susceptible individual. The object that carries the agent is often a fomite, an inanimate object. Think of someone sick sneezing, touching a door handle, then you, a susceptible person, touch that door handle and get sick. The door knob is a fomite. 2. Fecal-oral: Poop comes out and its contaminated. Then, you don't wash your hands, bite your nails, and end up with its contamination in your mouth. Think of when you reach into a bowl of candy at a restaurant. A pathogen is excreted in the feces of one individual and then ingested by another individual. 3. Respiratory, aka "aerosol": pathogens that replicate in the respiratory tract. 4. Vector-borne: transmitted by another species, like a mosquito carrying malaria that then parasites to humans 5. Sexual transmission Zoonotic transfers might also take place in which the pathogen moves from its natural host, its reservoir, to a human. Humans are typically "dead end" hosts, meaning the pathogen isn't efficiently transferred from person to person. Dead end means that the pathogen kills us, so we can't spread it to other humans.

Waht is normal flora? Why is normal flora good for us? How does birth affect a baby's normal flora? How does flora adapt to aging? What is our relationship with normal flora?

In a healthy host (like healthy us), the internal tissues are healthy and free from microorganisms, whereas surface tissues (like skin and mucous membranes) are constantly in contact with environmental organisms and become colonized by certain microbial species. The mixture of organisms regularly found at any anatomical site is called normal flora. We are literally COVERED in bacteria, like 10 lbs of those little guys. Why don't we get sick, say, when E. coli gets into a paper cut? Normal flora is responsible for helping us combat issues like this. The more infections you have when you're younger, the better off you are when you're older since your normal flora gains strength. Without normal flora present in our stomachs and intestines, we'd be dead! When a baby is born, it is germ-free. Then, after you come out of the vaginal canal, you take out some bacteria with you. You get exposed to E. coli, for the first time, when your mom puts her finger in your mouth and it accidentally has some fecal matter on it. Normal flora is affected by all of these things. Another point, breast-fed babies do better than bottle-fed babies because they get a different normal flora, one which is more combative against infection. Kids who are born through C-sections don't get exposed to the same bacteria from the vaginal canal, so their normal flora is different and they are more prone to infection. Normal flora is essential because it gives you things like vitamins, ecological stability, and helps your immunity develop. Normal flora changes as you age. It's transient. The relationship between us and normal flora is arguably commensal. It's really more mutualistic and symbiotic because we definitely do benefit from normal flora. On the other hand, however, some microorganisms that are normal flora can cause diseases or cancer.

What are the molecules used in invertebrate defense?

In an inflammation-like response, cytokines similar to IL-8 secreted by damaged cells can draw in immunity cells. There are some complement-like molecules. Some expression is induced by TLRs. Microbes are lysed in a manner similar to complement. There are many antimicrobial peptides and opsonization does take place, which assists in phagocytosis by hemocytes. Invertebrates lack the wide variety of specialized immune cells observed in vertebrates. They do have some cytoxic cells, some which are somewhat similar to NK cells. They also have phagocytes, particularly hemocytes. Hemocytes are the main line of invertebrate cellular immunity. They migrate through hemolymph, the blood of invertebrates, and into infected tissue areas. They bind foreign particles and ingest them. They produce toxic oxygen intermediates, antimicrobial peptides, and enzymes used to destroy pathogens. They can also differentiate into amoebocytes, secreting melanin for antimicrobial and clotting activities.

When did we know that we we had found ourselves in a problem with bacterial infections again? What are some reasons why we started to take some action?

In the late 80s, we began to notice an increase in bacterial infections and in 1995, we knew we were in trouble. Ted Kennedy and Bill Frisk were the two people who joined with Congress/Senate to make plans to do something. The US took action for 2 reasons: 1) An aging Population--More people took antibiotics-->More Drug Resistance --> More Infections. 2) The more you give out modern medications, the higher the increase in immune-compromised patients.

What is an early response of the body to infection?

Inflammation-an important, early physiologic response to microbial invasion and damage. It is triggered by the release of proinflammatory molecules like histamine and cytokines from local cells.

Compare and contrast the pros and cons of innate immunity versus acquired immunity.

Innate Pros: 1. Always on 2. Rapid response 3. No need for previous exposure since it is non specific. Innate Cons: 1. Can be overwhelmed 2. Lacks memory Acquired Pros: 1. Intense Response 2. Protects better on second exposure Acquired Cons: 1. Not "on" until exposed to foreign invader, since it's specific 2. Slow response-can take days-to-week to rise to full strength

What is considered the limiting element and a barrier to infection? What kind of reactions use this element?

Iron! Keeping iron for our cells is very important. We need iron for our own cells' function...but microbes also need iron to grow. Thus, we have to somehow use iron for ourselves but keep it from microbes. Several cell types make molecules to do this, to keep iron away from microbes. One example is lactoferrin, an iron binding protein that is found in the milk of mothers, tears, and saliva. Your body increases the expression of lactoferrin when a bacterial infection has struck. It keeps all the iron away from the bacterium to kill it. Redox reactions use irons.

What are the invertebrate defenses?

It appears to be only innate, using both cells and molecules. Most of what is known about it comes from research over a few model organisms like horseshoe crabs and fruit flies. There are strong similarities in the response and molecules used between vertebrates and invertebrates, however.

What bacteria does the complement kill?

It doesn't kill gram positive very well since they are pretty resistant with their huge levels of peptidoglycan. It can kill most gram-negative because there's a phospholipid bilayer and plasma membrane. Another reason why complement can kill gram negatives is because once a hole is made, lysozyme can go through and chew away the peptidoglycan. Envelope viruses can also be killed by complement. They have a membrane around their protein coat. Complement cannot kill parasitic worms or fungal pathogens.

What is LPS binding protein?

It is a protein found in the serum that is made by the liver and that floats around the entire body through the bloodstream. Its job is to look for lipopolysaccharide. When it sees it, it knows that you have a gram-negative infection and it brings that lipopolysaccharide then delivers it to TLR4.

What is a complement? What happens when a complement is activated?

It is also molecules of the innate system. A complement is a group of 30+ serum proteins involved in antimicrobial activities. Nine particular complement proteins become activated in a cascade in the presence of PAMPs. The activation of these 9 complement proteins results in: inflammation, opsonization (enhancing phagocytosis), and direct microbe killing through the formation of membrane-attack complex (MAC). The ultimate job of a complement protein is to form a MAC, which forms a pore in the bacterium and causes the bacterium to explode!

How would you describe the normal flora population?

It is both "transient" and resident. It is very abundant, with 10^14 individual normal flora compared to 10^13 body cells in a human.

Explain how polio is transmitted.

It is transmitted from a fecal-oral route. The virus is shed in the feces of infected persons. 95% of cases showed only a subclinical intestinal infection. 5% of cases showed a virus that spread and invaded the CNS, causing meningitis and sometimes paralysis. :(

What does activation of CD8+ cells produce?

It produces effector (killer) and memor cells. Killer cells recognize targets by their presentation of antigen epitope fragments on MHC class I. The T cells release perforin/granzyme to induce apoptosis in the target, thereby killing the target cell.

What cells first defend us against infectious agents?

Phagocytes: They are immune system cells that literally engulf foreign invaders. These include neutrophils, monocytes, and macrophages. Activation through PRRs and cytokine signaling turns these cells into efficient killing machines! Phagocytic and cytotoxic cells are the cellular effectors of innate immunity.

Why can't we use Koch's postulate and what is the alternative?

Koch's postulates can't be used today because we obviously can't go around injecting and killing people or animals with infectious diseases. So, we adapted new postulates. Molecular Koch's Postulates were proposed by Stanley Falkow: 1. Phenotype or property under association should be associated with pathogenic members of a genus or pathogenic strains of a species. The gene in question should be found in all pathogenic strains of the genus or species but be absent from nonpathogenic strains. (The virulence factor should be present in the pathogen). 2. Specific inactivation of the genes associated with the suspected virulence trait should lead to a measurable loss in pathogenicity or virulence (animal model). (Experimental inactivation of the virulence factor gene should lead to a decrease in virulence). 3. Reversion or allelic replacement of the mutated gene should lead to restoration of pathogenicity. (Experimental reversion of this inactivating change should result in restoration of virulence). 4. The gene, which causes virulence, must be expressed during infection. (The virulence factor should be expressed during an infection). 5. Immunity to the pathogen must provide protection.

Who was Koch?

Koch, in 1876, provided evidence for the "germ theory" of disease through his work with Bacillus anthracis and anthrax. He made "Koch's Postulate", a set of criteria to establish the cause of an infectious disease. Koch's postulates: 1. association of microbe with lesions of disease--He scraped the disease from a cow then view it under a microscope to see the bacterium. 2. Isolation of bacterium in pure culture 3. Show that the isolated bacterium causes disease in humans or animals--He injected the isolated bacterium into a sheep and killed it. 4. Re-isolation of bacterium from the intentionally infected animal-Isolate the bacterium from the dead animal and show it's the same as the bacterium you originally injected it with.

What is lysozyme?

Lysozyme is an enzyme that damages the cell wall of bacteria by catalyzing hydrolysis of the 1,4-B-linkages between GlcNAc (NAG) and MurNAc(NAM) residues in peptidoglycan. Lysozyme is a defense of the innate immune response and it is present in various secretions like tears, saliva, and mucus. It is also present in cytoplasmic granules released by PMNs.

What are MBL's and C-reactive protein?

MBL, or mannose=binding lectin, and C-reactive proteins are examples of opsonizing-secreted PRRs (pattern recognition receptors). MBL coats the mannose-rich surface of yeasts and bacteria. C-reactive protein binds to the phospholipids found in bacterial and fungal plasma membranes. Without the ability to make MBL, you have severe immunodeficiency.

Describe the antigen-presenting cells called macrophages.

Macrophages have the innate functions of phagocytosis and intracellular killing. Their professional APC (antigen presenting cell) functions include presentation to memoryy CD4+/CD8+ T-cells.

For each of these PRRs, tell me the molecule that it binds: MBL, C-reactive protein, LPS-binding protein, and compmlement factor C3b.

Mannose-binding Lectin (MBL): mannose of bacterial and fungal cell walls C-reactive Protein: Phsophatidylcholine/phosphocholine of bacterial and fungal membranes LPS-binding protein: Lipopolysacchardie (endotoxin) of gram-negative cell walls C3b complement factor: variety of cell-wall components, including lipoteichoic acid of gram-positive cell walls, and LPS of gram-negative bacteria

What are mast cells?

Mast cells are cytotoxic cells that release antihistamine. They are activated by PRRs and under degranulation to release granules that explode and kill the infectious cells.

What is the "dark side" of the immune system?

Septic shock might take place in which you have an overreaction to an infection to the point that you produce so much inflammation that you kill your body. Allergy or hypersensitivity is possible. Lastly, you could develop an autoimmune disease.

What do the majority of B cells recognize?

Most B cells recognize proteins. Proteins are by far the most immunogenic of the 3 types recognized by B cellls. Carbohydrates provide greater diversity but are not better receptors than proteins. Last of the three is lipids.

How are mucosal membranes a built-in barrier to infection?

Mucosal membranes are interior surfaces coated with wet mucus. Cilia move along the surface to prevent microbes from attaching. They also contain antimicrobial molecules like defensin proteins, lysozymes, and Lactoferrin. Just like in the skin, normal flora can colonize the mucosal membranes and "crowd out/starve out" potential microbial invaders.

Do a lot of microorganisms associated with humans cause disease?

No! Only a small proportion of them give rise to disease/cause a pathological change in spite of cell and tissue invasion. From an evolutionary standpoint, that makes sense. The microbes get what they need from living on our skin, then move on. To be a successful parasitic microbe, that's all you want to do, not to necessarily cause disease.

Is the local inflammatory response dangerous?

No, it's normal and done to protect the body. Systemic inflammatory response is the one to watch out for.

Explain the idea of carriers.

Not everyone who gets infected with something gets the disease. They are carrriers, in the carrier state, but they don't get the disease themselves. They might give it to someone, depending on the microorganism, or they might not. Carriers for TB, for example, never get the disease.

Why do we do booster shots?

The memory response or secondary/anamnestic response is much quicker than the primary response. This response is faster and more potent that the primary. Booster shots allow for minimal exposure to an infectious antigen, which allows for memory B cells to form and for faster adaptive immune response when secondary exposure eventually takes place.

Describe in 4 characteristics the innate immune response.

always active, non-specific, fast, no memory

Describe how B cells and T cells interact together.

Now you have a T cell. Each T cell's TCR can bind to one antigen. So the B cell and the T cell evolved to detect the SAME antigen because the B cell has its antibody receptors that's specific to this certain antigen and the T cell has its TCR that is specific. You can have more than one B cell or more than one T cell that detects that specific antigen, but each would have a different epitope. The one B cell finds this one T cell to activate each other to undergo clonal expansion. After the B cell binds and the TCR of the T cell, with the MHC class 2 complex of the B cell and the CD4 type of the T cell, binds with it, and activate each other, the B cell gets clonally expanded. Some clones become memory B cells and some will become effector B cells, or plasma B cells.

Give a run-down of how the two immune systems work to combat pathogens.

Once a microorganism has made its way into you, you have a quick host response (innate immunity), your body sounds the alarm, and then there are proteins that tell the rest of your body, "WE'RE IN TROUBLE!". Depending on whether or not you've seen the organism before or not, your adaptive response will kick in. This is a more focused attack on the organism attacking you at that very moment. It's specific.

What happens when lymphocytes are mature?

Once mature, lymphocytes are expelled into the peripheral blood stream as mature, naive lymphocytes. These cells migrate through lymphoid tissues distributed around the body, ready to respond to threats.

Describe the process of how phagocytosis works.

Opsonization (coating of cell) prior to ingestion enhances uptake. The contents of a neutrophil granule are released extracellularly and attack the invaders! Next, once the invader has been ingested, a complex process takes place to destroy it. Often, this destruction process involves fusion with lysosomes and the use of a controlled respiratory burst.

What is opsonization?

Opsonization is the coating of a protein, which enhances the destruction or uptake by other cells.

What happens to our adaptive immune response as we age and what 'fix' do we employ for this?

Our adaptive immune response starts to not work quite as well as it did before. Thus, you sometimes need a booster for certain vaccines. Your body is able to remember certain pathogens but not others.

What are PRRs? Are the relatively new? What type of recognition do they employ?

PRRs are Pattern Recognition Receptors, receptors on our cells that can bind to PAMPs to begin the responses against them. These receptors are evolutionarily ancient, as they are found in invertebrates, vertebrates, and plants. PRRs don't recognize molecules on individual pathogens, but rather, they recognize common molecules found on entire groups of pathogens. This is nonspecific recognition.

Describe the three associations possible between different organisms.

Parasitic: one benefits at the expense of another (EX: measles, typhoid, tuberculosis) Mutualistic/Symbiotic: both organisms benefit (EX: microflora inhabiting rumen os cows) Commensalism: one organism benefits, but not at the expense of the other; difficult to see this category with confidence (EX: bacteria living on skin)

Define pathogenesis, infection and specific signs/symptoms.

Pathogenesis: mechanism of a microbe with disease production Infection: replication of a pathogen in or on its host Specific Signs: responses associated with a specific disease

Define phagocytosis, phagocyte, phagosome, phagolysosome, and lysosome.

Phagocytosis: ingestion of foreign particles by a cell Phagocyte: host cell adapted specifically to engulf and destroy bacteria or other foreign particulate matter Phagosome: vacuole resulting from ingestion of particulate material by phagocytes Phagolysosome: vacuole resulting from fusion of phagosome and lysosome Lysosome: mammalian cell granule contaiining hydrolytic enzymes and other compounds toxic to bacteria

Define phagocytosis, receptor-mediated endocytosis, and pinocytosis.

Phagocytosis: takes in large objects (whole bacteria) Receptor-mediated Endocytosis: initiated by binding of particles to cell-surface receptor molecules Pinocytosis: "drinking" in small extracellular volumes containing macromolecules

Describe what happens to intracllular antigens and the endogenous pathway.

Proteasomes fragment the intracellular antigens. The resulting small peptide fragments are transported to the endoplasmic reticulum, then loaded onto MHC class I molecules. Presentation is therefore restricted to CD8+ cytotoxic T cells that can bind to MHC class I structures. The MHC I:peptide complexes are transported to the Golgi apparatus. Membrane fusion of vesicles from the Golgi aparatus places MHC I:peptide complex on cell surface.

Which diseases are still prevalent today?

Respiratory infections, AIDS, diarrheal diseases, TB, Malaria and measles

How is skin a built-in barrier to infection? Which bacteria do well on skin?

Skin is typically inhospitable to foreign microbes. It is cool, dry, and acidic. Skin has a dead layer on top that serves as an 'armor'. On top of that is an antimicrobial oil (sebum). Oils are made of fatty acids that are inhabitory to many microorganisms. Sweat secretions can further provide antimicrobial barrier. Additionally, normal flora might colonize the skin and crowd out/starve out potential invaders. The skin also has very tight junctions in the epithelial layers with proteins that keep the layers together. So if you're a pathogen trying to break your way in, you have to be able to break through these tight junctions. Gram-positive bacteria do well on skin. Gram negatives need more moisture and are more susceptible to fatty acids and lipids killing them.

What are the built-in barriers to infection?

Skin! Mucosal Membranes! Lysozymes! Iron!

Describe the different types of organisms in terms of what diseases they cause.

Some organisms cause a single, well-defined disease state. For example, Treponmea pallidum always causes syphilis. Plasmodium species always cause the one disease of malaria. In MOST cases, however, one organism can lead to multiple manifestations of disease. Staphylococcus auerus can cause endocartitis, pneumonia, wound infections, or food poisoning. And, many types of organisms produce the same disease. So, for example, meningitis can be caused by viruses, bacteria, fungi, and parasites.

Describe the adaptive immune defense.

The adaptive immune defense is found ONLY in vertebrates, but works with the innate responses to achieve a stronger level of defense. However, unlike the innate system, it recognizes SPECIFIC pathogens instead of broad classes of microbes. The response is mediated by molecules that bind to specific pathogens. After initial exposure to a pathogen, the adaptive immune system retains MEMORY of the response used and can initiate it more quickly (and more effectively) upon re-exposure. It is ADAPTIVE because it gets better with each exposure.

What are the 2 different types of pathogens?

Strict/Primary Pathogens are organisms that are always associated with a certain disease. Opportunistic pathogens are organisms that are typically members of normal microbial flora, but can establish disease when found in unprotected sites within the human hosts, like the bloodstream. E. coli, for example, normally lives in our intestines without causing any damage, but it could cause disease if it got into our blood stream. Another example is a sinus infection caused from normal microflora.

What are the central cells in adaptive immunity?

T-cells! Through initiation of adaptive immunity is complex and multiple cell types are involved, T cells are involved with the cell-mediated side of adaptive immunity.

What are TLRs?

TLRs, Toll-LIke Receptors, are a form of PRR (pattern recognition receptors) found in vertebrates and invertebrates. They were originally described in fruit fly embryos. They are transmembrane proteins that recognize PAMP ligands and trigger an internal signaling reaction in self cells.

What happens to the released complement proteins?

The "b's" tend to stay and work. The body has evolved ways to use the other parts that are released as signals to warn the immune response that it needs to kick in with action. Complement proteins are used to signal the body for an immune response They are signals for HELP!

What are the consequences of local inflammation?

Vasodilation Extravasation Increase in Vessel Permeability These consequences signal for the immune cells to be brought in, like phagocytes, to fight the infection. Cytokines are often used to communicate the status of an injection. They produce fever, enhance inflammation, and stimulate further immune responses.

Instead of coating the surface of the cell with antibodies, what is another way that opsonization takes place?

The complement protein, C3b, flaots of fand binds to certain structures on the bacterium. The phagocytic cell has receptors for C3b, so phagocytosis can take place much more efficiently because it can recognize the bacterium with the C3b complement proteins attached.

Describe the innate immune defenses.

The innate immune defenses, also called the quick host response, is found in all multicellular organisms. It provides a first line of defense against microbes and typically recognizes biochemical differences between microbes and host cells. While microbes can be recognized as "foreign," this system CAN'T discern the precise identity of the microbe. It simply responds to an entire group of similar microbes in the same manner. It is "nonspecific" in the nature of its responses.

In terms of the morphology and lineage of cells involved in the immune response, what is the difference between the lymphoid tract and the myeloid tract?

The lymphoid tract is mainly here the adaptive immune responses come from. The T and B cells are associated with the lymphoid tract. The myeloid tract is associated with the innate response and involves phagocytic cells.

How does a macrophage stop and travel to the correct blood vessel even with the flow of blood pushing it along?

The macrophage stops and makes it to the correct blood vessel because there are receptors made by the body that these macrophage cells are able to grab onto and stop at.

Describe the immune system. What are the main organs/tissues of it?

The main job of the immune system is to protect us from microbial infection. Immunity literally means "exempt". It's a relatively new study area, just a bit over 100 years. The main organs and tissues of the immune system = BLPS-blood, lymphatic system, primary lymphoid tissue (bone marrow, thymus) & secondary lymphoid (spleen, mucosa-associated lymphoid tissue)

Describe memory cells and the memory response.

The memory response works faster and faster, as fast as it can, in your body. The memory T cells establish memory of previous exposure, a hallmark of adaptive immunity. Memory cells differentiate during the initial adaptive immune responses. Memory cells are long-lived, produce a faster and more vigorous response when the same antigen is encountered again, and the speed of the 2nd, 3rd, or 4th response can even present a repeat infection from occurring.

What was the miracle drug, what did it treat, and why did our miracle drug innately fail us?

The miracle drug was antibiotics. The nickname "miracle drug" first came about because the antibiotic was the first thing to treat streptococcus pneumoniae. Our miracle drugs failed us because, with time, we developed a sense of invincibility. We thought that bacterial infections and other key infectious organisms were no longer a threat and our attention was turned to other health issues like cancer, heart disease, and HIV/AIDS.

What are the different types of MHC cells?

There are 2 types: MHC class I and MHC class II. Every mammal has some sort of MHC-like response. In humans, it is also called the HLA response-human leukocyte activation.

How is the complement cascade activated?

There are 3 different methods: 1. Classical-1st one discovered but not the most prevalent. An antibody needs to bind to the surface structure of the organism in order to activate the pathway. An example is an LPS antibody binding to the surface, causing the complement to get activated. At least 2 antibodies must bind. 2. Alternative Pathway: evolutionary older, It is LPS specific so it can bind to gram negatives or gram positives. C3B can bind directly to LPS and activate the complement cascade. 3. Lectin: similar to the classical pathway; Mannose-binding lectin will bind to the mannose and activate the complement. Each of these methods activate the complement cascade. Once the complement is activated, inflammation, opsonization, or MAC can occur!

What are the antimicrobial compounds of lysosomes and their effects?

There are 3: 1. Lysozyme: hydrolysis of peptidoglycan of the bacterial cell wall = killing action 2. Proteases: degradation of proteins = killing action 3. Defensins: form pores in bacterial membranes = killing action; These are a form of antimicrobial peptides!!!

What are super antigens?

There are awful killers called super antigens that bypass this controlling step and cause for every T cell to get activated. You end up dying a horrible death where all of your skin peels off. Lots of bacteria and virus make these super antigens.

What is one problem with phagocytosis?

There's a limit on how much a cell can take in and ingest through phagocytosis. It isn't a cure for everything. A macrophage, for example, cannot eat a parasitic worm.

How are adaptive immune responses initiated?

They are initiated through exogenous antigens and the endocytic pathway. Extracellular antigens are taken in by endocytosis. Extracellular antigens are taken in by endocytosis. Once the antigens have been taken into the inside of the cell, the cell has to present it, tell the other cells "hey guys, I've got an antigen that's not supposed to be here." If it's on the inside, then it's broken down and presented on MHC class II. This restricts presentation to CD4+ T cells that can bind to MHC class 2 structures. Once presented, this initiates the activation of helper T cells.

What are Type 1 interferons?

They are molecules of the innate system and there are 2 kinds: interferon alpha and interferon beta. They are induced by viruses and can initiate a natural antiviral state. Over 300 genes increase expression when exposed to Type I interferons! They also can increase the activities of antiviral cells, or NK cells. If you have a viral infection, the goal of the interferon is to tell the cell being invaded and all of the neighboring cells that there is a virus near by and that these cells need to start changing by altering their gene expression in order to stop growing and spreading the virus. Even if it means killing the cells, that is better than allowing the virus to spread and infect more cells. If the interferon response is large, then your cells will begin to degrade ANY RNA. Type I interferons can also inhibit ribosomal binding, which prevents the host cell protein production. By changing membrane components, these interferons block viral attachment and entry. Basically, the interferon response shuts down the host cell.

What are antibacterial peptides? How do they not kill you?

They are peptides which exist everywhere in the mucosal surfaces of the body. Their job is to attack bacterial membranes and prevent them from invading the body. They are able to do this because they are typically positively charged, or cationic. They don't kill you because the yaer specific. Gram negative and gram positive bacteria both have fully negatively charged surfaces, meaning they're anionic. Thus, antibacterial peptides can fully recogize them and kill 'em. Our cells, on the other hand, are more neutral, not really pos or neg charged. Our cells produce cholesterol, a neutral lipid, that isn't made in bacteria. Lastly, the phospholipids in bacteria are anionic while ours are cationic. Thus, antibacterial peptides don't recognize our cells as needing to be killed. Antibacterial peptides recognize bacteria, bind to their surfaces, and then organize into pores before lysing the bacteria. They make a lot of pores. One problem is that pathogens which are trying to kill you can sometimes sense these peptides and respond by changing the surface of their cell so that they aren't recognized. Gram-negative bacteria will change the LPS molecule and cleaves off its phosphate groups.

How do some bacterial cells beat the opsonization/phagocytosis system?

They have evolved to be able to live in the phagosome and never die. They prevent acidication and lysozomal fusion. Complement cannot kill the bacteria and antbiodies can't attach to the bacteria. Basically, they evade the immune response.

How does a pathogen go about causing a disease? Where do pathogens begin?

To cause disease, a pathogen must attach and enter the host. 95% of infectious diseases begin on mucous membranes of respiratory, GI, and urogenital tracts. There is a mucosal layer that they can cling to. Thus, most diseases are respiratory or gastrointestinal. The other 5% of infectious diseases start from vector bites, like mosquitoes. Most have a mechanism for breaking the skin.

Describe the evolution and drug resistance of tuberculosis.

Today, tuberculosis is thought of as being basically untreatable due to total drug-resistance. People used to be TERRIFIED of TB because it was wiping out entire families, so it became a law that you had to get TB vaccinated. By the 40s and 50s, TB was under control. But by the 70s, we stopped all screening processes and stopped educating our doctors about TB, thinking that we had successfully beat the disease. We relied on electronic imaging, not screening. Then, throughout the Regan years, many of the psych patients were released, who ended up on the streets, and living in terrible conditions. As a result, TB manifested itself again. We developed a new vaccination for it and tried to get rid of it, but once we did, just like before, we got too close for comfort and let the situation become too relaxed. Thus, TB dismantled again and here we are, now on our 4th strain of TB vaccine.

Describe why vasodilation comes as a consequence to local inflammation.

Vasodilation-increased blood flow, a response that takes place in order to get more red blood cells OUT in an attempt to fight the infection. There are parts on the surface of bacteria or virus that tell your body that it has an infection. This leads to the projection of molecules that act as vasodilators like cytokines. Bacteria continue to grow in their early stage. If you are not doing a good enough job of fighting it, they will make more surface molecules that alert your immune system, which lends to further vasodilation. You begin to swell at the source of infection and increased blood flow causes the redness to spread.

What are the 2 main types of transmission?

Vertical transmission-An infected parent makes a first generation who is exposed to the disease by ovum, sperm, or placenta, or when the child is born, it gets exposed to the disease by contact with parent or milk intake. An example of vertical spread is commensal bacteria. Horizontal spread takes place with infected air, water, food, contact, vectors, etc. Examples of horizontal spread are polio, influenza, and typhoid. Horizontal transfer is the transmission of a pathogen between members of a species other than parent to offspring.

What is virulence? What is a CI ration? How does this relate to pathogens?

Virulence is a measure of a disease a pathogen can induce. CI is a case-to-infection ratio, a proportion of infected individuals who develop the disease. Pathogens can weaken over time or show different virulence levels due to genetic differences. Attenuated strains show decreased virulence, which may be useful for vaccine development. Avirulent strains can no longer cause diseases.

How do we sense or detect the presence of pathogens?

We use Pathogen-Associated Molecular Patterns, or PAMPs. PAMPs allow the innate immune system to determine what is foreign and what is not. PAMPs are found on foreign microbes but are not on self cells.

Describe the classical activation method of activating the complement cascade. How are the alternative and lectin activation pathways different?

When you activate the 1st protein in complement, C1 is only activated if it is cross-linked between 2 antibodies. Following after is a series of proteolytic events. Eventually, you reach the point where you cleave a protein that is key in the complement cascade, C5, which allows you to insert into the membrane attack complex (MAC). If enough MAC is inserted into a cell membrane, the cell explodes! A deficiency in any one of the complement proteins could alter a patient's ability or way to fight a disease. The lectin and alternative pathways are slightly different. While their endgame is still MAC insertion, the activation at the beginning is slightly different.

What is the difference, in terms of virulence, between small pox and poleo?

With small pox, all people infected show symptomms so treating it is much easier than treating polio. Only about 5% of people with polio actually show symptoms, so eradicating this disease is very expensive and difficult.

How do you kill a virus that lives inside of one of your cells?

You can't use a phagocytic cell since that wouldn't recognize the intracellular virus. You can use a natural killer, NK, cell. They are cytotoxic and are useful for eliminating infected host cells. They can kill one cel since many healthy cells are saved and we are multicellular organisms. While they aren't phagocytic, they do make direct contact with target cells. After contact is initiated, granule components are released . These granules contain various components to kill the target cell. NK cells are also useful for eliminating abnormal self-cells like cancer.

How can you determine if something is microbial or not?

You evolve receptors that only bind key features of microbes. For example, PAMPs on bacteria, flagella, LPS, peptidoglycan, etc.

How does the memory tool of the acquired immunity system work?

You have already evolved millions of T-cells and B-cells to help look for invaders. They are stored, but when your body is invaded, it tries to find a match and when there is a match, your body takes action with a huge immune response to get it out.

What happens when you get an infection in regards to cytokines?

You produce proinflammatory molecules like histamines and cytokines. Cytokines are molecules that tell the immuno-infectors what to do. They sound the alarm. You could die if the immune system goes a-wall and produces too many cytokines. Cytokines are small proteins that are used to tell other immuno-cells where the site of infection is and to bring cells to that sit

What is the IGE response?

the IGE response is a type of antibody that causes for less mast cells to be released when an organism is infected with worms. People that have been exposed to worms have less IGE floating around, lending to less mast cell release, which causes less of a histamine response.