Chapter 21: Immune system

Surface barriers use protective chemicals that inhibit or destroy microorganisms. What are the four ways this is achieved?

1. Acidity, of skin and secretions (acid mantel, inhibits growth) 2. Enzymes - Lysozyme of saliva, respiratory mucus, and lacrimal fluid... All of these kill microorganisms! *pew pew* 3. Defensins - Antimicrobial peptides that inhibit growth 4. Other chemicals - Lipids in sebum, dermcidin in sweat which is an antimicrobial toxin

There are two populations of T cells, what are they? Do T cells activate other T cells? Is a Naive T cell called a T cell?

(The two populations of T cells are based on which glycoprotein surface receptors are displayed.) 1. CD4 cells usually become *helper T cells* (Th). These activate B cells, other T cells, macrophages and also direct an adaptive immune response. Some CD4 cells become regulatory T cells (Suppressor T cells), this moderate immune response. CD4 cells can also become Memory T cells 2. CD8 cells become *cyotoxic T cells* (Tc), these bad boys destroy cells harboring foreign antigens and also become memory T cells. Yes! Helper, cytotoxic, and regulatory T cells are activated by T cells. A naive T cell is called CD4 or CD8 cells.

What does the inflammatory response do?

(it is triggered whenever body tissues are injured.) -Prevents spread of damaging agents -disposes of cell debris and pathogens -alerts adaptive immune system -sets the stage for repair

What happens when surface barriers are breached by nicks or cuts, and microorganisms invade deeper tissues?

-Our second line of defense must protect deeper tissues which include: 1. Phagocytes 2. Natural killer cells 3. Antimicrobial proteins (interferons and complement proteins) 4. Fever 5. Inflammatory response, which include: Macrophages, mast cells, WBCs, and inflammatory chemicals.

what are complete antigens functions?

Immunogenicity: the ability to stimulate proliferation of specific lymphocytes (pretty much the ability to stimulate cells and CREATE weapons!) Reactivity: the ability to react with activated lymphocytes and antibodies released by immunogenic reactions (pretty much the ability to USE the weapons that we are making.)

Inflammatory response: Edema

Increased capillary permeability, which results in *Exudate* to tissues. Moves foreign material into lymphatic vessels and delivers clotting and complement proteins. Exudate is fluids that leak around the cells of the capillaries that caused inflammation. These fluids contain clotting factors and antibodies. This also causes local swelling (edema!). The swelling pushes on nerve endings which results in pain. Pain can also be a result from bacterial toxins, prostaglandins, and kinins.

Surface barriers are apart of which system? what defense do they provide?

Innate defense. Surface barriers ward off invading pathogens (IE: Skin, mucous membranes and their secretions) They provide a physical barrier to most microorganisms. Keratin (in the skin) is resistant to weak acids and bases, bacterial enzymes and toxins. Lastly mucosae provides similar mechanical barriers.

What are interferons and what do they do?

Interferons are a family of immune modulating proteins, that have slightly different physiological effects. Viral-infected cells secrete IFNs (alpha or beta) to "warn: neighboring cells. These IFNs enter neighboring cells, and produce proteins that block viral reproduction and degrade viral RNA. IFN alpha and beta also activate Natural Killer cells. (The "interferon" is a sinking ship that sends out all of its seamen to other boats and they build up defense from the pirates!)

What are two Antimicrobial proteins

Interferons or IFNs and complement proteins. They 1. attack microorganisms directly and 2. hinder microorganisms ability to reproduce. (The good old 1-2 combo! Interfere than complement!)

what does maturation mean?

Mature means educated Immunocompetence means lymphocytes can recognize one specific antigen by binding to it. B or T cells display unique receptors on surface when they achieve maturity, they can bind to only 1 antigen. Self-tolerance means lymphocytes are unresponsive to their own antigens. AKA they will not attack self!

What is the fate of clones?

Most clones become plasma cells. They secrete specific antibodies at the rate of 2000 molecules per second for 4 to 5 days then they die. Clone cells that do not become plasma cells are memory cells. They provide our immunological memory. They also mount an immediate response when they are exposed to the same antigen. Antibodies circulate the blood or lymph. They will bind to free antigens and mark them for destruction by innate or adaptive mechanisms.

What do vaccines do?

Most vaccines contain dead or very weak (attenuated) pathogens. This spares us the symptoms of the primary response and provides antigenic determinate that are immunogenic and reactive. Vaccines may result in the illness you are trying to vaccinate. May cause an allergic response.

What are some surface barrier modifications for the respiratory system?

Mucus-coated hairs in the nose Cilia of upper respiratory tract sweep dust and bacteria-laden mucus towards the mouth.

Natural Killer Cells

NK cells are nonphagocytic, large granular lymphoctyes that attack cells that lack "self" cell-surface receptors. All of our healthy cells have a "self" receptor (imagine our healthy self cells wearing birthday cone hats!), when a cell becomes infected by a pathogen, it stops producing that receptor (Its hat falls of!!) If a NK cell see's a cell with out the "self" (b-day hat) receptor, it will induce apoptosis (programed cell death! ouch!). This is very important in cancer cells and virus-infected cells. NK cells also secrete potent chemicals that enhance the inflammatory response.

What is neutralization?

Neutralization is the simplest defensive mechanism! Antibodies will block specific sites on viruses or bacterial exotoxins. Antibodies binding will prevent these antigens from binding to receptors on tissue or cells Antigen-antibody complexes undergo phagocytosis

Phagocyte mobilization! (Call for arms!! Order of arrival)

Neutrophils lead the way (first responders) and macrophages follow after. As the attack continues monocytes will arrive. The macrophages can arrive up to 12 hours after pathogens have left the blood stream. (this one is slide 21, open for interpretation) The late arrivers replace the dying neutrophils and remain for clean up before we repair/heal.

Do antigens determines which foreign substances the immune system will recognize?

Nope! Genes actually determine which foreign substances the IS will recognize. Immune cell receptors are the result of acquired knowledge of microbes likely in the environment. (immunity = memory, we have receptors of microbes we have killed. Almost like how the predator keeps skulls as trophy, our receptors our are trophies) Lymphocytes make up to a billion different types of antigen receptors (Trophies! they are awesome killers). These receptors are coded by about 25,000 genes

When a lymphocyte binds and becomes activated it transform(differentiates) into what? (hint 3 things)

Once activated it can PROLIFERATE, which is an exact clone of its self. Most of the clones will actually be plasma cells (effector cells) that do all the heavy hitting and fights the infection. Some become memory cells, these make us able to respond to the same antigen again more quickly the next time we encounter it. (they are the Ripley of lymphocytes, she knows aliens, memory cells know antigens.)

antigenic determinants

Only certain parts (antigenic determinants) of entire antigen are immunogenic Antibodies and lymphocyte receptors bind to them as enzyme binds substrate (Antigenic determinants are basically different shaped receptors on the end of an antigen. which different antibodies bind to. IE. one antigen has a 3 receptors: a triangle, square and oval. 3 different types of antibodies will have to bind to each with a matching receptor)

What is passive humoral immunity? What are the two types?

PHI, is readymade antibodies introduced into the body. B cells are not challenged by antigens. Immunological memory does not occur. The protection ends when antibodies degrade 1. Naturally acquired, antibodies delivered to fetus via the placenta(IgG) or to the infant through milk(IgA) 2. artificially acquired, would be an injection of serum such as gamma globulin (the protection is immediate but ends when the antibodies naturally degrade in our body)

What is Precipitation?

Precipitation is soluble molecules are cross-linked. (soluble antigens) Complexes precipitate and are subject to phagocytosis.

Self-antigens: MHC proteins

Protein molecules (self-antigens) on the surface of cells are not antigenic to its self but antigenic to others in transfusions or grafts. One group of self-antigens are called MHC glycoproteins There are millions of possible combinations The two major classes of MHC proteins are: Class I MHC proteins, these are found on virtually all cells in the body EXCEPT RBC's. Class II MHC proteins on the other hand are ONLY found on certain cells in the immune response (antigen present cells)

What is immunity?

Resistance to disease

What is the Complement system?

~20 blood proteins that circulate in inactive form our cells contain complement activation inhibitors. Enhances both innate and adaptive defenses unleashes inflammatory chemicals that amplify all aspects of inflammatory response promotes phagocytosis kills bacteria and certain other cell types by cell lysis. These have to be activated.

What to T cells provide defense against? How do T cells defend against antigens?

T cells provide defense against *Intercellular* antigens Some T cells directly kill cells, others release chemicals that regulate an immune response to deal with (even though we haven't been beaten by machines, T cells are kind of like a Machine, they will kill or figure out a way to fix the problem that is inside the cell)

Where and how do T cells mature? About how many are made this way?

T-cells mature in the thymus. They can mature two ways known selection pressures (or tests) These two selections happen in order! 1. Positive selection, selects a T cell that is capable of recognizing self-MHC proteins (MHC restriction); those that fail this process are destroyed by apoptosis! (basically if a T cell recognizes a self-MHC, it gets to move to step 2) 2. Negative selection, prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC. Negative selection ensures self-tolerance (aka negative selection kills T cells that would attack ourself/cause autoimmune disease. The T cell must not bind tightly to self-antigens) Over all only about 2% of T cells survive this selection process.

What are adaptive defenses?

The adaptive defense system are our 3rd line of defense, it attacks particular foreign substances. -This takes longer to react than the innate system. -Adaptive has to be activated (turned on)

Is the innate defense systemic or local?

The innate defense is both systemic and local!

Do Regulatory T cells amplify or dampen immune response? How? What is an important function of T-reg Cells?

They dampen immune response by: direct contact and inhibitory cytokines. Regulatory T cells are important in preventing autoimmune reactions. They suppress self-reactive lymphocytes in periphery (outside lymphoid organs)

What do Cytotoxic T cells do? (Tc) Once activated are they stationary or mobile? What do cytotoxic cells target? How do Cytotoxic cells kill? What other cells use the same methods to KILL?

They directly attack and kill other cells. Once activated Tc cells circulate in the blood, lymph and lymphoid organs in search of body cells displaying an antigen they recognize Tc cells target: 1. Virus-infected cells 2. Cells with intracellular bacteria or parasites 3. cancer cells 4 foreign cells (transfusions or transplants. not self) Tc kill via two methods: 1. They release perforins (Create pores through which granzymes can enter the target cell) and granzymes (Stimulate apoptosis) by exocytosis. 2. They bind to specific membrane receptor on a target cell and stimulates apoptosis. *Natural killer cells* use the same key mechanisms as Tc for killing target cells.

What are the roles of Helper T(Th) cells? What would immune response would happen with out Th (helper T) cells?

They play a central role in the adaptive immune response. They activate both humoral (B cells!) and cellular arms. Once primed by APC, in the presence of an antigen they: 1. Help activate T and B cells 2. Induce T and B cell proliferation 3. Their cytokines recruit other immune cells NONE!! with out helper T cells there is no immune response.

What are the cells of the adaptive immune system? (hint there are 3)

Two of the 3 types are lymphocytes: B Lymphocytes (B cells) - humoral immunity T lymphocytes (T cells) - Cell-mediated immunity The third type are Antigen-presenting cells (APCs), APCs do not respond to specific antigens and play an essential auxiliary role in immunity

What are adaptive defenses?

We have a few types of adaptive defenses. Specific - recognizes and targets specific antigens Systemic - these defenses are not restricted to the initial site (body wide) We memory defenses that have stronger attacks to "known" antigens (antigens we have encountered before. Memory leads to immunity via B & T cells) There are two separate but overlapping arms: Humoral and cellular. Humoral (antibody-mediated) immunity (B-cell) Cellular (cell-mediated) immunity (T-cell)

What is active humoral immunity. What are the two types?

When B cells encounter antigens and produce specific antibodies against them There are two types of active humoral immunity: 1. Naturally acquired, the Immune system responses to bacterial or viral infections (fighting it off the old fashioned way) 2. Artificially acquired: The immune system responses to a vaccine of dead or attenuated (living but really really weakened) pathogens

Can B cells switch antibody classes?

Yes, be cells can switch antibody classes but retain their antigen specificity. For example you can make a IgM and then later it turn into a IgG. Almost all secondary responses are IgG

What does MHC stand for?

major histocompatibility complex

process/mechanism of phagocytosis

pathogens are killed by acidifying and digesting via lysosomal enzymes. Helper T cells cause the release of enzymes that produces the *Respiratory burst,* which kills pathogens that are resistant to lysosomal enzymes. The "Burst" does this by; Releasing cell-killing free radicals, Producing oxidizing chemicals (H2O2), and Increasing pH and osmolarity of phagolysosome. Defensins (in neutrophils) pierce membrane [Look more into this?]

What are two types of MHC proteins that are important to T cell activation/What cells recognize them?

1. Class I MHC proteins, these are displayed by all cells *EXCEPT* RBCs. This protein is recognized by CD8 (another name for a niave Tc) cells. 2. Class II MHC proteins, these are displayed by APCs ,(Dendritic cells, macrophages, and B cells) and recognized by CD4 (niave helper T cells) cells

phagocyte mobilization: What are the order of events from when we are injured?

1. Leukocytosis: release of neutrophils from bone marrow in response to Leukocytosis-inducing factors from injured cells. (the LIF is the fire alarm the injured cells hit!) 2. Margination: Neutrophils cling to walls of capillaries in inflamed area in response to CAMs (cell adhesion molecules). (The neutrophils hug the wall of capillary like a fire fighter taking cover before going around the corner) 3. Diapedesis: Neutrophils squeeze through capillary walls and begin phagocytosis (The fire fighter neutrophils have to squeeze through some falling debris, before they can get to the fire. They than start EATING the fire to put it out) 4. Chemotaxis: Inflammatory chemicals (chemotactic agents) promote positive chemotaxis of neutrophils. This is just the neutrophils following the trail of inflammation, which keeps them on the right path. (The fire fighter neutrophils keep putting out the fire because they can see the embers [chemotaxis] keeping them on the right path) Chemotaxis is a positive feed back loop, we will stop once the job is done.

What are the two big Phagocytes in the immune system?

1. Neturophils, are the most abundant but die while fighting. They become phagocytic upon exposure to infectious material. 2. Macrophages, develop from monocytes. They are the chief phagocytic cells, very robust! -Macrophages can be free floating or fixed inside some organs. -free floating macrophages move through tissue spaces, e.g. alveolar macrophages -fixed macrophages are permanent residents of some organs; e.g., kupffer cells (liver) and microglia (brain)

what are the order of events during T cell activation? specifically proliferation and differentiation.

1. Primary T cells response peaks within a week. 2. T cells apoptosis occurs between days 7 and 30. (The benefit of apoptosis is that activated T cells are actually hazardous. They produce large amounts of inflammatory cytokines, which could result in Hyperplasia and cancer!) 3. Effector activity wanes as amount of antigen declines. 4. Memory T cells remain and mediate future secondary responses.

Describe the order of events of the adaptive defense in humoral Immunity (Humoral = B cell)

1. Primary response (initial encounter with an antigen, aka the bad guy) 2. Antigens will bind with a receptor of a specific B lymphocyte. IMPORTANT: this is the antigen challenge when binding happens (Some B lymphocytes may not have a matching/complementary receptor and remain inactive) 3. B cell is activated and clones its self. 4. The B cells become either Plasma cells ( also called Effector B cells, that secrete antibody molecules into the blood stream. Basically free floating defense for the antigen it just killed) or memory B cells (ready to fight the same antigen again)

What are the Cardinal signs of Inflammatory Response?

1. Redness 2. Heat. 3. Swelling 4. Pain (sometimes 5. impairment of function)

With immunological memory describe the difference between the primary response and secondary response.

1. The primary immune response results in cells proliferation and differentiation upon first exposure to an antigen. The lag period is 3 to 6 days (during this time building up clones, plasma cells and memory cells) The peak level of plasma cell antibody is reach in 10 days, after that the antibody level declines (the plasma cells die off) 2. The secondary immune response is the RE-exposure to the same antigen. The response is faster, more effective and prolonged. Sensitized memory cells respond with in hours of contact. Antibody levels peak in 2 to 3 days at much higher levels than first exposure. Antibodies bind with a greater affinity and antibody levels can remain high for weeks to months.

Do antigen-antibody complexes destroy antigens? Do antibodies invade solid tissues? Do antibodies act inter-cellularly?

1. antigen-antibody complexes do not destroy antigens. They prepare them for destruction by innate defense! 2.No antibodies do not invade solid tissues UNLESS lesion is present. 3. Yes, but only IF they are attached to a virus before it enters a cell (this will activate mechanisms that destroy the virus)

Lymphocyte development, maturation, and activation: What are the 5 (general) steps

1. origin - all originate in red bone marrow 2. maturation 3. seeding secondary lymphoid organs and circulation 4. antigen encounter and activation 5. proliferation and differentiation

What are the five classes Immunoglobulins (Ig also antibodies) and what do they do?

1.IgM - The *first antibody released*. It is a potent agglutinating agent. It readily fixes and activates complement. *Has the HIGHEST avidity (affinity)*, IgM is found on the surface of B cells as receptors 2.IgA(secretory IgA) - *Found in mucus and other secretions including saliva, tears, and colostrum (found in breast milk)*. IgA helps prevent early entry of pathogens 3.IgD - Attached to the surface of B cells, *functions as a B cell receptor.* 4.IgG - Monomer; 75-85% of antibodies in plasma. Form secondary and late primary responses. *Crosses placental barrier*, *Most abundent Ig. 5IgE - Monomer active in some allergies (type 1 hypersensitivity) and parasitic infections. IgE mediates type 1 hypersensitivity by causing mast cells and basophils to release histamine. IgE defends against parasitic worms by causing eosinophils to produce worm destroying enzymes.

What are the two types of immune system defense?

1.Innate (nonspecific) 2. Adaptive (specific) Both are intrinsic systems

What is the ratio of T cells to B cells?

3:1

What is a it mean when you call a B or T cell Naive? How do B and T cells enter circulation?

A naive B or T cell are immunocompetent, not yet exposed to antigens. B and T cells are exported from the primary lymphoid organs (bone marrow and the thymus), and "seed" secondary lymphoid organs (lymph nodes, spleen..ect). (Seeding is just entering other lymphs, and they are still naive, but entering the circulation increases their chances of an encounter with an antigen. They pretty much move out of their home and start looking for bad guys)

what is the mechanism of phagocytosis?

A phagocyte must adhere to the particle it wants to destroy. (Some microorganisms evade adherence with capsules) Opsonization, marks pathogens for deletion, coating by complement proteins or antibodies which promote phagocytosis. (This just puts more binding sites on a pathogen, making it easer for a phagocyte to nom nom it)

Antigen-presenting cells (APCs) Function and types

APCs engulf antigens and present fragments of antigens to T cells so they can recognize them later. The major types include: 1.Dendritic cells, that live in connective tissue and epidermis 2.Macrophages, can be found in connective tissues and lymphoid organs 3.B cells

what is a Fever?

Abnormally high body temperature systemic response to invading microorganisms leukocytes and macrophages that are exposed to foreign substances secrete Pyrogens Pyrogens act on the bodies thermostat via the hypothalamus thus raising the body temp. (fever is almost like when there is too much foreign substances for the leukocytes and macrophages to handle so they release the P bomb (pyrogens) which tell the hypothalamus to burn the patogens up!)

What is agglutination?

Agglutination is when antibodies bind to the same determinant on more than one cell-bound antigen (Imagine a antibodies is Y shaped, it has 3 points to bind to that antigen. so one antibody bound to multi antigens) Cell-bound antigens. Cross-linked antigen-antibody complexes agglutinate -an example: clumping of mismatch blood cells.

What are antibodies?

Antibodies are proteins also know as Immunoglobulins - gamma globulin are a portion of blood. Antibodies are capable of binding specifically with antigens detected by B cells.

What are antibodies targets and functions?

Antibodies inactivate and then tag antigens. They do not destroy them. This forms antigen-antibody (immune) complexes. Defensive mechanisms used by antibodies: are neutralization and agglutination (These at the two most important!), Precipitation and complement fixation. How can we remember this? PLAN! Precipitation, Lysis (by complement), Agglutination, Neutralization.

what are Antigens

Antigens are substances that can mobilize adaptive defenses and provoke an immune response in our body. antigens are targets of all adaptive immune responses. Antigens are "antibody generators"

Where do B and T cells come from? and where do they mature?

B and T cells are made in red marrow B cells mature in the bone marrow T cells mature in the thymus

Where do B cells mature? How are they selected? What happens if B cells are self-reactive?

B cells mature in red bone marrow. If B cells escape from the bone marrow they are INACTIVATED (anergy). B cells are positively selected if they can successfully make antigen receptors. If a B cell is reactive (attacks self), it is destroyed by apoptosis (clonal deletion), or the B cell will undergo "receptor editing". Receptor editing is simply the rearrangement of their receptors (our body saying here lets fix that for you.)

Do eosinophils attack worms or allergies?

Both. This could be a tricky question I bet.

C-reactive protein (CRP)

CRP is produced by the liver in response to inflammatory molecules. CRP is a clinical marker used to assess: 1. the presence of an acute infection 2. An inflammatory condition and its response to treatment. If a treatment is working, the CRP should be going down.

What kind of immunity comes from T lymphocytes?

Cell-mediated immunity

What is clonal selection?

Clonal selection is kind of what it sounds like. A naive lymphocyte cell has its first encounter with an antigen (this is called the antigen challenge remember!), and proceeds to develop further. If the right bind happens the lymphocyte will start to different. (CLONES!!)

What are cytokines? What are examples of cytokines? What do other cytokines do? How is IL-1 released, and what does it do? What is IL-2? What does it do?

Cytokines are the chemical messengers of the immune system. They mediate cell development, differentiation, and responses in the immune system. Interferons and interleukins (IL-1) are cytokines! Other cytokines amplify and regulate innate and adaptive responses. EG: Tumor necrosis factor - cell toxin EG: Gamma interferon - enhances killing power of macrophages Interleukin 1 is released by macrophages and it will co-stimulate bound T cells to: 1. Release interleukin 2 (IL-2) 2. Synthesize more IL-2 receptors. IL-2 is a key growth factor, it acts on cells that release it (IL-2) and other T cells. 1. IL-2 encourages activated T cells to divide rapidly. 2. IL-2 is used therapeutically to enhance the body's defense against cancer (melanoma and of the kidney)

dendritic cells and macrophages

Dendritic cells phagocytize pathogens, then enter lymphatics to present antigens to T cells in lymph nodes. These guys are the most effective antigen presenters, they can also activate naive T cells. Their whole job is to kill something and bring whats left over home. Macrophages are widespread in lymphoid organs and connective tissues. They can activate naive T cells also! They present antigens to T cells to activate themselves into voracious phagocytes that secrete bactericidal chemicals

The adaptive defense is faster than the innate defense system? T/F

False, the adaptive takes longer.

What are innate defenses?

First: external body membranes (skin and mucosae) Second: (internal) Antimicrobial proteins, phagocytes, Natural killer cells, antimicrobial proteins, fever. -Innate is active all the time (always on) -The second line of defense inhibits spread of invaders; inflammation is the most important mechanism here.

What is complement fixation and activation? What are activated complement functions?

Fixation and activation is the main antibody defense against cellular antigens (bacteria, mismatched RBCs) Several antibodies bind close together on a cellular antigen, complement-binding sites on stem regions align. Tiggers complement fixation into cells surface, cell lysis. Activated complement functions include: Amplifies inflammatory response, promotes phagocytosis via opsonization, positive feedback cycle that enlists more and more defensive elements.

Haptens (Incomplete Antigens)

Haptens are small molecules that are not immunogenic by themselves. They are partial antigens, and can make a self antigen look like a non-self antigen(eg. peptides, nucleotides, some hormones) Haptens may be immunogenic if they are attached to body proteins and combination is marked foregin Haptens cause the immune system to mount harmful attacks (this is a hypersensitive reaction) Examples of haptens are: poison ivy, animal dander, detergents and cosmetics.

How do helper T cells amplify the innate defenses?

Helper T cells amplify the response of innate immune system by activating macrophages which results in more potent killers. They also mobilize lymphocytes and macrophages and attract other types of WBCs (Helper T cells is kind of like Forerunner of the empire for the Innate defense system, brings out the attackers makes the enrage happen aka higher kill potential!)

How do helper T cells activate B cells? Can B cells be activated without Helper T cells? HOW!? Do most antigens need Th?

Helper T cells stimulate B cells to divide more rapidly and begin antibody formation. B cells may be activated with out Th (helper t) cells by binding to T cells-independent antigens (this response is weak and short-lived) Yes, Most antigens require Th (helper T) co-stimulation to activate B cells: T cell-dependent antigen

What are the benefits and dangers of fevers?

High fevers are dangerous because they can denature enzymes The benefits of a moderate fever are 1. causes liver and spleen to hold onto/store iron and zinc (aka the microorganisms/foreign invaders food) and 2. increases metabolic rate which results in faster repair (aka everything is working harder)

What immunity does adaptive defenses provide?

Humoral immunity (B-cells) Cellular immunity (T-cells)

What type of immunity comes from B Lymphocytes? Do they activate T cells?

Humoral immunity, No they do not activate naive T cells. B cells present antigens to helper T cells that assist in their own activation

what is interferon gamma?

IFN gamma (immune interferon), is secreted by lymphocytes, casus widespread immune mobilizing effects and finally activates macrophages! (IFN Gamma is like a steroid for macrophages, it makes them better/stronger killers) Since beta and alpha IFN activate NK cells and macrophages, gamma indirectly fight cancer. artificial IFNs used to treat hepatitis C, genital warts, multiple sclerosis, hairy cell leukemia.