ch 21 ap

Explain how a T cell is activated.

-Immunocompetent T cells are activated when their surface receptors bind to a recognized antigen

Cell Mediated Immune Response

-Since antibodies are useless against intracellular antigens, cell-mediated immunity is needed -Two major populations of T cells mediate cellular immunity: -CD4 cells (T4 cells) are primarily helper T cells (TH) -CD8 cells (T8 cells) are cytotoxic T cells (TC) that destroy cells harboring foreign antigens

a graft that is transplanted from one person to a genetically identical individual (i.e., to an identical twin) is an example of

an isograft -An autograft is transplantation of a tissue from one location to another in the same person; an allograft is a graft between different members of the same species; and a xenograft is made between two different species.

MHC II proteins are found on

antigen presenting cells

b lymphocytes

humoral immunity

When are phagocytes active?

-Phagocytes are active in the presence of antigens.

leukocytosis

An increase in the number of white blood cells that are in circulation -Leukocytosis. Injured cells release chemicals called leukocytosis-inducing factors. In response, neutrophils enter blood from red bone marrow and within a few hours, the number of neutrophils in blood increases four- to fivefold. This leukocytosis, the increase in white blood cells (WBCs), is characteristic of inflammation.

which of the following minerals needed for bacterial reproduction do both the liver and spleen sequester during a fever

iron and zinc -Fever is an adaptive response that seems to benefit the body, but exactly how it does so is unclear. Fever causes the liver and spleen to sequester iron and zinc, which may make them less available to support bacterial growth. Additionally, fever increases the metabolic rate of tissue cells, and may speed up repair processes.

which statement below is characteristic of a secondary humoral response

it occurs much more rapidly than a primary response -If (and when) someone is reexposed to the same antigen, whether it's the second or twenty-second time, a secondary immune response occurs. Secondary immune responses are faster, more prolonged, and more effective, because the immune system has already been primed to the antigen, and sensitized memory cells are already "on alert." These memory cells provide immunological memory.

what fever inducing molecules are secreted by leukocytes and macrophages

pyrogens -Inflammation is a localized response to infection, but sometimes the body's response to the invasion of microorganisms is more widespread. Fever, an abnormally high body temperature, is a systemic response to invading microorganisms. When leukocytes and macrophages are exposed to foreign substances in the body, they release chemicals called pyrogens (pyro = fire). These pyrogens act on the body's thermostat—a cluster of neurons in the hypothalamus—raising the body's temperature above normal [37°C (98.6°F)]. Fever is an adaptive response that seems to benefit the body, but exactly how it does so is unclear. Fever causes the liver and spleen to sequester iron and zinc, which may make them less available to support bacterial growth. Additionally, fever increases the metabolic rate of tissue cells, and may speed up repair processes. Antibodies are secreted by plasma cells, while histamine and heparin are secreted by mast cells. Keratin is a protein found in the skin.

the property of lymphocytes that prevents them from attacking the body's own cells

self-tolerance -Each lymphocyte must be relatively unresponsive to self-antigens so that it does not attack the body's own cells. This is called self-tolerance. Immunogenicity is the ability to stimulate specific lymphocytes to proliferate. Immunocompetence is the ability of a lymphocyte to recognize its specific antigen by binding to it. Immunological memory is carried out by immune cells that have been previously sensitized to an antigen so they can respond to the next exposure very quickly.

Explain the clonal selection and differentiation of B cells. Where do the B cells become immunocompetent and how does this occur?

- B cells become immunocompetent in the bone marrow because thats where they mature. -Clonal selection is a theory stating that B cells express antigen-specific receptors before antigens are ever encountered in the body.

macrophages

A common antigen presenting cell (APC) -Antigen-presenting cells (APCs) engulf antigens and then present fragments of them, like signal flags, on their own surfaces where T cells can recognize them. Naive T cells can only be activated by antigens that are presented to them on MHC proteins by APCs. In other words, APCs present antigens to the cells that will deal with the antigens. The major types of cells acting as APCs are dendritic cells, macrophages, and B lymphocytes. Macrophages are widely distributed throughout the lymphoid organs and connective tissues. Although macrophages, like dendritic cells, can activate naive T cells, macrophages often present antigens to T cells for another reason—to be activated themselves. Certain effector T cells release chemicals that prod macrophages to become activated macrophages. Activated macrophages are true "killers"—insatiable phagocytes that also trigger powerful inflammatory responses and recruit additional defenses. Many lymphocytes coordinate both humoral and cellular adaptive immune responses. B lymphocytes differentiate into plasma cells, which secrete immunoglobulins (antibodies). Mast cells bind IgE produced by plasma cells in response to allergens, and cause inflammation when the IgE on the surface of the cell is cross-linked by an allergen.

which of the following defines opsonization

A process of coating a pathogen to enhance phagocytosis. -Molecules released during complement activation tremendously amplify the inflammatory response and promote phagocytosis via opsonization. This sets into motion a positive feedback cycle that enlists more and more defensive elements.

which of the following is a characteristic of a secondary immune response

A secondary immune response lasts longer than a primary immune response. -If (and when) someone is reexposed to the same antigen, whether it's the second or twenty-second time, a secondary immune response occurs. Secondary immune responses are faster, more prolonged, and more effective, because the immune system has already been primed to the antigen, and sensitized memory cells are already "on alert." These memory cells provide immunological memory.

cytotoxic t cells

Attack and lyse cells that are not "self" -When activated, CD4 and CD8 cells differentiate into the three major kinds of effector cells of cellular immunity. CD4 cells usually become helper T (TH) cells that help activate B cells, other T cells, and macrophages, and direct the adaptive immune response. CD8 cells become cytotoxic T (TC) cells that destroy cells in the body that harbor anything foreign. Some CD4 cells become regulatory T (TReg) cells, which moderate the immune response. Activated CD4 and CD8 cells can also become memory T cells. Note that the names of the effector cells (helper, cytotoxic, regulatory) are reserved for activated T cells, while naive T cells are simply called CD4 or CD8 cells.

which of the following describes hyperemia

Increased blood flow due to vasodilation of blood vessels entering the injured area -Vasodilation accounts for two of the cardinal signs of inflammation. The redness and heat of an inflamed region are both due to local hyperemia (congestion with blood) that occurs when local arterioles dilate. Excess blood flow to an area will cause local swelling, or edema. The fluid that seeps out of the blood vessels and contains clotting factors and antibodies, is called exudate. The white blood cells (leukocytes) that leave in exudate are attracted to the site of injury/inflammation by chemotaxis.

neutrophils

Phagocytes; will migrate to the site of an infection within a few hours -Neutrophils, the most abundant type of white blood cell, become phagocytic on encountering infectious material in the tissues. Neutrophils and other WBCs migrate up the gradient of chemotactic agents to the site of injury. Within an hour after the inflammatory response has begun, neutrophils have collected at the site and are devouring any foreign material present. Macrophages are leukocytes derived from circulating monocytes. Natural killer (NK) cells, part of the innate response, attack cancerous cells. Plasma cells, derived from B lymphocytes, secrete antibodies.

all of the following describes interferons except that

they are virus-specific -Viruses—essentially nucleic acids surrounded by a protein envelope—lack the cellular machinery to generate ATP or synthesize proteins. They do their "dirty work" in the body by invading tissue cells and taking over the cellular metabolic machinery needed to reproduce themselves. Infected cells can do little to save themselves, but some can secrete small proteins called interferons (IFNs) (in"terfēr' onz) to help protect cells that have not yet been infected. The IFNs diffuse to nearby cells, which they stimulate to synthesize proteins that "interfere" with viral replication in still-healthy cells by blocking protein synthesis and degrading viral RNA. Because IFN protection is not virus-specific, IFNs produced against a particular virus protect against other viruses, too. The IFNs are a family of immune modulating proteins produced by a variety of body cells, each having a slightly different physiological effect. IFN alpha (α) and beta (β) have the antiviral effects that we've just described and also activate natural killer (NK) cells. Another interferon, IFN gamma (γ), or immune interferon, is secreted by lymphocytes and has widespread immune mobilizing effects, such as activating macrophages. Because both macrophages and NK cells can also act directly against cancerous cells, the interferons have an indirect role in fighting cancer. Genetically engineered IFNs are used to treat several disorders including hepatitis C, genital warts, and multiple sclerosis.

Discuss fever and why a moderate fever is beneficial. (second line of defense)

-Abnormally high body temperature in response to invading microorganisms -Leukocytes and macrophages exposed to bacteria and other foreign substances secrete pyrogens -High fevers are dangerous because they can denature enzymes (proteins) (changes form therefore removes function) -Moderate fever can be beneficial, as it causes: -The liver and spleen to sequester iron and zinc (needed by microorganisms) -An increase in the metabolic rate, which speeds up tissue repair

Antibodies

-Also called immunoglobulins -Are soluble proteins secreted by activated B cells and plasma cells in response to an antigen -Are capable of binding specifically with that antigen

Humoral Immune Response

-Antigen challenge - first encounter between an antigen and a naive immunocompetent cell -Takes place in the spleen, lymph node or other lymphoid organ -If the lymphocyte is a B cell: -The challenging antigen provokes a humoral immune response -Antibodies are produced against the challenger

Describe the different types of tissue grafts used in transplants. Give an example of each.

-Autografts - graft transplanted from one site on the body to another in the same person -Isografts - grafts between identical twins -Allografts - transplants between individuals that are not identical twins, but belong to same species -Xenografts - grafts taken from another animal species

Discuss active immunity, both naturally and artificially acquired, and give an example.

-B cells encounter antigens and produce antibodies against them -Naturally acquired - response to a bacterial or viral infection -Artificially acquired - response to a vaccine of dead or attenuated pathogens

Explain the inflammatory response. (Second line of defense)

-Begins with a flood of inflammatory chemicals released into the extracellular fluid -Chemicals liberated by the inflammatory response increase the permeability of local capillaries -Exudate—fluid containing proteins, clotting factors, and antibodies (at the site of the injury) -Exudate seeps into tissue spaces causing local edema (swelling), which contributes to the sensation of pain -increase in blood flow to the area causing the swelling, heat. redness, pain

Explain immunodeficiency. Give an example.

-Congenital and acquired conditions in which the function or production of immune cells, phagocytes, or complement is abnormal -Hodgkin's disease - cancer of the lymph nodes leads to immunodeficiency by depressing lymph node cells -Acquired immune deficiency syndrome (AIDS) - cripples the immune system by interfering with the activity of T cells -Characterized by severe weight loss, night sweats, and swollen lymph nodes -Opportunistic infections occur, including pneumocystis pneumonia and Kaposi's sarcoma

Discuss passive immunity, both naturally and artificially acquired, and give an example.

-Differs from active immunity in the antibody source and the degree of protection -B cells are not challenged by antigens -Immunological memory does not occur -Protection ends when antibodies naturally degrade in the body -Naturally acquired - from the mother to her fetus via the placenta -Artificially acquired - from the injection of serum, such as gamma globulin

Immunocompetent B or T cells

-Display a unique type of receptor that responds to a distinct antigen -Become immunocompetent before they encounter antigens they may later attack -Are exported to secondary lymphoid tissue where encounters with antigens occur -Mature into fully functional antigen-activated cells upon binding with their recognized antigen -It is genes, not antigens, that determine which foreign substances our immune system will recognize and resist

Explain phagocytosis.

-Foreign particle (antigen) adheres to the phagocyte (macrophage) -Pseudopods (extension of cytoplasm) engulf the particle (antigen) into a phagosome (vesicle inside of the macrophage that contains the antigen) -Phagosomes fuse with a lysosome to form a phagolysosome -Antigens in the phagolysosome are digested by proteolytic (digestive- come from the lysosome) enzymes -Indigestible and residual material is removed by exocytosis

List the five classes of antibodies and their functions

-IgD -attached to the surface of B cells, important in B cell activation -IgM -released by plasma cells during the primary immune response -IgG -most abundant and diverse antibody in primary and secondary response; crosses the placenta and confers passive immunity -IgA -helps prevent attachment of pathogens to epithelial cell surfaces -IgE -binds to basophils, causing histamine release when activated

Explain the difference between innate and adaptive immunity.

-Innate (nonspecific) system responds quickly and consists of: -First line of defense - skin and mucosae prevent entry of microorganisms -Second line of defense -phagocytes and inflammatory response -Inhibits spread of invaders throughout the body -Adaptive (specific) defense system -Third line of defense - mounts attack against particular foreign substances -Takes longer to react than the innate system -Works in conjunction with the innate system

Explain autoimmune diseases. Give an example.

-Loss of the immune system's ability to distinguish self from nonself -The body produces autoantibodies and sensitized T cells that destroy its own tissues -Examples include multiple sclerosis, myasthenia gravis, Graves' disease, Type I (juvenile) diabetes mellitus, systemic lupus erythematosus (SLE), glomerulonephritis, and rheumatoid arthritis

NK cells & antimicrobial proteins

-NK cells (Natural killer cells) -Non specific granular lymphocytes -Release chemicals to lyse cancerous and virus infected cells -Antimicrobial proteins -Interferon -Complement -Complement is a group of plasma proteins (present in blood plasma) which destroy foreign substances (nonspecific)

Describe the function of a phagocyte.

-Phagocytes are cells that protect the body by ingesting harmful foreign particles, bacteria, and dead or dying cells. -Main phagocytic cells are macrophages

Compare the primary and secondary immune response

-Primary immune response - cellular differentiation and proliferation, which occurs on the first exposure to a specific antigen -Lag period: 3 to 6 days after antigen challenge -Peak levels of plasma antibody are achieved in 10 days -Antibody levels then decline -Secondary immune response - re-exposure to the same antigen -Sensitized memory cells respond within hours -Antibody levels peak in 2 to 3 days at much higher levels than in the primary response -Antibodies bind with greater affinity, and their levels in the blood can remain high for weeks to months

Explain the roles of the skin in the innate defense. (first line of defense)

-Skin and mucous membranes make up the first line of defense -Epithelial membranes produce protective chemicals that destroy microorganisms -Skin acidity (pH of 3 to 5) inhibits bacterial growth -Keratin in the skin: -Presents a physical barrier to most microorganisms (water proofing) -nonspecific so it attacks any kind of pathogen -acts very quickly

Explain the roles of mucous membranes in the innate defense. (first line of defense)

-Stomach mucosae secrete concentrated HCl and protein-digesting enzymes (too acidic for anything to live) -Mucus (made by goblet cells) traps microorganisms that enter the digestive and respiratory systems -Mucus-coated hairs in the nose trap inhaled particles -Mucosa of the upper respiratory tract is ciliated -Cilia sweep dust- and bacteria-laden mucus away from lower respiratory passages -nonspecific so it attacks any kind of pathogen -acts very quickly

Define antigen.

-Substance that can mobilize the immune system and provoke an immune response -Examples: -Common cold virus -Influenza virus (vaccine also) -Pollen -Microorganisms -Splinter

Explain the clonal selection and differentiation of T cells. Where do the T cells become immunocompetent?

-T cells become immunocompetent in the thymus because thats where they mature. -In clonal selection, an antigen is presented to many circulating naive B and (via MHC) T cells, and the lymphocytes that match the antigen are selected to form both memory and effector clones of themselves.

What determines which specific antigens our immune system will be able to recognize?

-T cells must simultaneously recognize: -Nonself (the antigen) -Self -Provides the key for the immune system to recognize the presence of intracellular microorganisms

adaptive immune defenses

-The adaptive immune system: -Recognizes specific foreign substances -Acts to immobilize, neutralize, or destroy foreign substances -Amplifies inflammatory response and activates complement -The adaptive immune system is antigen-specific, systemic, and has memory -It has two separate but overlapping arms: -Humoral, or antibody-mediated immunity -Cellular, or cell-mediated immunity -takes longer to react because it is specific and attacks specific antigens

What is the function of the inflammatory response?

-The inflammatory response is triggered whenever body tissues are injured (cut, scrape, burn) -Prevents the spread of damaging agents to nearby tissues -Disposes of cell debris and pathogens -Sets the stage for repair processes -The four cardinal signs of acute inflammation are redness, heat, swelling, and pain

Why are the internal defenses called the second line of defense?

-The second line of defense are the non-specific phagocytes and other internal mechanisms that comprise innate immunity. (phagocytes, inflammatory response, fever, NK cells, antimicrobial proteins) -This is what kicks in if something penetrates the skin or mucous membrane (the first line of defense)

Inflammatory Response: Edema

-The surge of protein-rich fluids into tissue spaces (edema): -Helps dilute harmful substances -Brings in large quantities of oxygen and nutrients needed for repair -Allows entry of clotting proteins, which prevents the spread of bacteria

xenograft

A tissue or organ graft between different species. -A transplant from one location to another in the same person is called an autograft. Congenital thymic aplasia is an immune deficiency disease in which the thymus fails to develop. Affected individuals have no T cells, and so have little or no immune protection; fetal thymic and bone marrow transplants have been helpful in some cases. Eczema is a clinical term for several conditions that cause "weeping" skin lesions and intense itching. One common cause, atopic dermatitis, has a strong familial predisposition, has features of immediate hypersensitivity, and usually begins in the first five years of life. Recent research suggests the underlying defect may be increased leakiness of the skin. Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder that occurs mainly in young females. Septic shock (sepsis) is a dangerous condition in which the inflammatory response goes out of control.

which of the following describes edema

Caused by excess tissue fluid in the injured area; helps to dilute harmful substances and brings in excess oxygen -Inflammatory chemicals also increase the permeability of local capillaries. Consequently, exudate—fluid containing clotting factors and antibodies—seeps from the blood into the tissue spaces. This exudate causes the local swelling (edema) that presses on adjacent nerve endings, contributing to a sensation of pain. Pain also results from the release of bacterial toxins, and the sensitizing effects of released prostaglandins and kinins. Aspirin and some other anti-inflammatory drugs reduce pain by inhibiting prostaglandin synthesis. Although edema may seem detrimental, it isn't. The surge of protein-rich fluids into the tissue spaces sweeps foreign material into lymphatic vessels for processing in the lymph nodes. It also delivers important proteins such as complement and clotting factors to the interstitial fluid.

which is correctly matched

Cytotoxic T cells: activated by antigens bound to MHC I -Cytotoxic T (TC) cells (activated CD8 cells) are the only T cells that can directly attack and kill other cells. TC cells roam the body, circulating in and out of the blood and lymph and through lymphoid organs in search of body cells displaying antigens that the TC cells recognize. Their main targets are virus-infected cells, but they also attack tissue cells infected by certain intracellular bacteria or parasites, cancer cells, and foreign cells introduced into the body by blood transfusions or organ transplants. Before the onslaught can begin, the cytotoxic T cell must "dock" on the target cell by binding to a self-nonself complex. Remember, all body cells display class I MHC antigens, so TC cells can destroy all infected or abnormal body cells. The attack on foreign human cells, such as those of a graft, is more difficult to explain because here all of the antigens are nonself. However, apparently the TC cells sometimes "see" the foreign class I MHC antigens as a combination of self class I MHC protein bound to foreign antigen.

what is the definition of exudate

Fluid that seeps from the capillary containing clotting factors and antibodies during inflammation -Inflammatory chemicals also increase the permeability of local capillaries. Consequently, exudate—fluid containing clotting factors and antibodies—seeps from the blood into the tissue spaces. This exudate causes the local swelling (edema) that presses on adjacent nerve endings, contributing to a sensation of pain. Pain also results from the release of bacterial toxins, and the sensitizing effects of released prostaglandins and kinins. Aspirin and some other anti-inflammatory drugs reduce pain by inhibiting prostaglandin synthesis.

which of the following is mismatched

Helper T cells: directly target and kill cancer cells -When activated, CD4 and CD8 cells differentiate into the three major kinds of effector cells of cellular immunity. CD4 cells usually become helper T (TH) cells that help activate B cells, other T cells, and macrophages, and direct the adaptive immune response. CD8 cells become cytotoxic T (TC) cells that destroy cells in the body that harbor anything foreign. Some CD4 cells become regulatory T (TReg) cells, which moderate the immune response.

plasma cells

Produce immunoglobulins -Plasma cells develop the elaborate internal machinery (largely rough endoplasmic reticulum) needed to secrete antibodies at the unbelievable rate of about 2000 molecules per second. Each plasma cell functions at this breakneck pace for 4 to 5 days and then dies. The secreted antibodies, each with the same antigen-binding properties as the receptor molecules on the surface of the parent B cell, circulate in the blood or lymph. There they bind to free antigens and mark them for destruction by other innate or adaptive mechanisms. APCs, or antigen presenting cells, can be any one of several types of cells, e.g., dendritic cells, macrophages, B cells, that present digested antigen for recognition by T cell. Mast cells release histamine and heparin when the IgE bound to their surface is cross-linked. This produces an inflammatory response.

chemotaxis

The process by which white blood cells are attracted to the site of an injury -Inflammatory chemicals act as homing devices, or more precisely chemotactic agents. Neutrophils and other white blood cells (WBCs) migrate up the gradient of chemotactic agents to the site of injury. Within an hour after the inflammatory response has begun, neutrophils have collected at the site and are devouring any foreign material present.

immunity gained through injections of dead or attenuated strains of the disease-causing agents

active artificial -When your B cells encounter antigens and produce antibodies against them, you are exhibiting active humoral immunity. Active immunity is acquired in two ways. It is (1) naturally acquired when you get a bacterial or viral infection, during which time you may develop symptoms of the disease and suffer a little (or a lot), and (2) artificially acquired when you receive a vaccine. Indeed, once researchers realized that secondary responses are so much more vigorous than primary responses, the race was on to develop vaccines to "prime" the immune response by providing a first encounter with the antigen.

immunity gained from being exposed to the pathogen and developing the illness

active natural -When your B cells encounter antigens and produce antibodies against them, you are exhibiting active humoral immunity. Active immunity is acquired in two ways. It is (1) naturally acquired when you get a bacterial or viral infection, during which time you may develop symptoms of the disease and suffer a little (or a lot), and (2) artificially acquired when you receive a vaccine. Indeed, once researchers realized that secondary responses are so much more vigorous than primary responses, the race was on to develop vaccines to "prime" the immune response by providing a first encounter with the antigen.

immediate hypersensitivity

allergy -Immediate hypersensitivities, also called acute or type I hypersensitivities, are simply what most of us would call allergies (allo = altered; erg = reaction). An allergen is an antigen that causes an allergic reaction. Allergic reactions begin within seconds after contact with the allergen and last about half an hour. The initial meeting with an allergen produces no symptoms but it sensitizes a susceptible person, causing IgE antibodies to be secreted that attach to the surfaces of the body's mast cells and basophils. Later encounters with the same allergen trigger an allergic reaction, in which the allergen promptly binds and cross-links the IgE antibodies on the surfaces of the mast cells and basophils. This event induces an enzymatic cascade. Mast cells and basophils release a flood of histamine and other inflammatory chemicals that together induce the inflammatory response typical of allergy. Allergic reactions may be local or systemic (bodywide). Mast cells are abundant in connective tissues of the skin and beneath the mucosa of respiratory passages and the gastrointestinal tract, and these areas are common sites of local allergic reactions.

when collagen fibers are laid down to wall off a sac of pus, what structure is formed

an abscess -In severely infected areas, the battle takes a considerable toll on both sides, and creamy yellow pus (a mixture of dead or dying neutrophils, broken-down tissue cells, and living and dead pathogens) may accumulate in the wound. If the inflammatory mechanism fails to clear the area of debris, collagen fibers may be laid down, which walls off the sac of pus, forming an abscess. The abscess may need to be surgically drained before healing can occur.

humoral immunity is provided by

antibodies -Humoral immunity, also called antibody-mediated immunity, is provided by antibodies present in the body's "humors," or fluids (blood, lymph, etc.). Though they are produced by lymphocytes, antibodies circulate freely in the blood and lymph, where they bind primarily to extracellular targets—bacteria, bacterial toxins, and free viruses—inactivating them temporarily and marking them for destruction by phagocytes or complement.

substances that can trigger the adaptive defenses and provoke an immune response

antigens -Antigens are substances that can mobilize the adaptive defenses. They are the ultimate targets of all adaptive immune responses. (Antigen is a contraction of "antibody generating.") Most antigens are large, complex molecules (natural or synthetic) that are not normally present in the body. Consequently, as far as our immune system is concerned, they are intruders, or nonself. Antibodies are proteins produced by plasma cells to bind to antigens and help clear pathogens from the body. Haptens, incomplete antigens, by themselves are not immunogenic. Interleukins are soluble molecules that allow communication between cells involved in the immune system.

this type of disease results from the inability of the immune system to distinguish self from nonself-antigens

autoimmune disease -Occasionally the immune system loses its ability to distinguish friend (self) from foe (foreign antigens). When this happens the artillery of the immune system, like friendly fire, turns against itself. The body produces antibodies (autoantibodies) and cytotoxic T cells that destroy its own tissues. This puzzling phenomenon is called autoimmunity. If a disease state results, it is referred to as autoimmune disease. Some 5% of adults in North America—two-thirds of them women—are afflicted with an autoimmune disease. You have encountered examples of autoimmune diseases in earlier chapters, and you will encounter more later on. Some important autoimmune diseases are: Rheumatoid arthritis, which systematically destroys joints Myasthenia gravis, which impairs communication between nerves and skeletal muscles Multiple sclerosis, which destroys the myelin of the white matter of the brain and spinal cord Graves' disease, which prompts the thyroid gland to produce excessive amounts of thyroxine Type 1 (insulin-dependent) diabetes mellitus, which destroys pancreatic beta cells, resulting in a deficit of insulin and inability to use carbohydrates Systemic lupus erythematosus (SLE), a systemic disease that particularly affects the kidneys, heart, lungs, and skin Glomerulonephritis, which damages the kidney's filtration membrane and severely impairs renal function An allergy is an acute, or type I hypersensitivity, to an allergen. When this response is severe and system-wide, it is called anaphylaxis - a potentially life-threatening condition. SCID, severe combined immunodeficiency syndrome, is a congenital immunodeficiency in which children have little or no protections against disease-causing organisms.

self-reactive B cells are eliminated in the

bone marrow -Lymphocytes are "educated" (go through a rigorous selection process) as they mature. The aim of this education is twofold: Immunocompetence. Each lymphocyte must become able (competent) to recognize its one specific antigen by binding to it. This ability is called immunocompetence. When B or T cells become immunocompetent, they display a unique type of receptor on their surface. These receptors (some 105 per cell) enable the lymphocyte to recognize and bind a specific antigen. Once these receptors appear, the lymphocyte is committed to react to one (and only one) distinct antigenic determinant because all of its antigen receptors are the same. The receptors on B cells are in fact membrane-bound antibodies. The receptors on T cells are not antibodies but are products of the same gene superfamily and have similar functions. Self-tolerance. Each lymphocyte must be relatively unresponsive to self-antigens so that it does not attack the body's own cells. This is called self-tolerance. Maturation is a two- to three-day process that occurs in the bone marrow for B cells and in the thymus for T cells. Recall that the lymphoid organs where lymphocytes become immunocompetent—thymus and bone marrow—are called primary lymphoid organs. All other lymphoid organs are referred to as secondary lymphoid organs.

cytotoxic T cells kill target cells

by inserting perforins into the target's membrane -Once cytotoxic T cells recognize their targets, how do they deliver a lethal hit? There are two major mechanisms. One involves perforins and granzymes (Figure 21.19). The other involves binding to a specific membrane receptor on the target cell that stimulates the target cell to undergo apoptosis. NK cells, introduced earlier, use the same key mechanisms to kill their target cells. Natural killer (NK) cells, however, do not look for foreign antigen displayed on class I MHC proteins. Instead they search for other signs of abnormality, including the lack of class I MHC or the presence of antibodies coating the target cell. Stressed cells also often express different surface markers, which can activate NK cells. In short, NK cells stalk abnormal or foreign cells in the body that TC cells can't "see." NK cells and TC lymphocytes roam the body, adhering to and crawling over the surfaces of other cells, examining them for markers they might recognize, a process called immune surveillance. NK cells check to make sure each cell has "identity flags" (class I MHC proteins inhibit NK cell attack), whereas TC cells check the "identity flags" to see if they look the way they are supposed to (foreign antigens stimulate TC cell attack).

t lymphocytes

cell-mediated immunity

which of the following inflammatory processes attracts neutrophils to the injured area

chemotaxis -Neutrophils and other white blood cells (WBCs) migrate up the gradient of chemotactic agents to the site of injury. Within an hour after the inflammatory response has begun, neutrophils have collected at the site and are devouring any foreign material present. Leukocytosis is an abnormally high number of leukocytes. Leukocytes in the vicinity of inflammation/injury will begin slowing down and marginating, and then cross the blood vessel wall by the process of diapedesis.

the process that begins when a helper T cell binds to a class II MHC protein on a displaying cell is known as

co-stimulation -Once antigen binding has occurred, the T cell is stimulated but is still "idling," like a car that has been started but not put into gear. Before an "idling" T cell can be "put into gear" and proliferate to form a clone, it must also bind one or more co stimulatory signals. These signals are yet other molecules that appear on the surfaces of APCs in tissues that are damaged or invaded by pathogens. For example, dendritic cells and macrophages sprout co-stimulatory molecules on their surfaces when the innate defenses are being mobilized. The binding of these molecules to specific receptors on a T cell is a crucial costimulatory signal. What happens if a T cell binds to antigen without receiving the co-stimulatory signal? In this case, the T cell becomes tolerant to that antigen and is unable to divide or secrete cytokines. This state of unresponsiveness to antigen is called anergy. The two-signal sequence acts as a kind of "double-handshake," a safeguard to prevent the immune system from destroying healthy cells. Without this safeguard, class I MHC proteins, which occur on all body cells and which display peptides from within the cell, could activate cytotoxic T cells, leading to widespread damage of healthy cells. The important thing to understand is that along with antigen binding, co-stimulation is crucial for T cell activation. To go back to our idling car analogy, the car will not go anywhere unless it has been both (1) started and (2) put into gear.

which of the following is not a surface barrier to pathogen influx

complement cascade -As show in the table below, skin secretions, mucous membranes, and saliva/tears all contribute to surface membrane barriers while the complement cascade does not.

macrophages

derived from circulating monocytes -The most voracious phagocytes are macrophages ("big eaters"), which derive from white blood cells called monocytes that leave the bloodstream, enter the tissues, and develop into macrophages. Free macrophages wander throughout the tissue spaces in search of cellular debris or "foreign invaders." Fixed macrophages, like stellate macrophages in the liver, are permanent residents of particular organs. Neutrophils are the 'first responders' at sites of injury. Nautral killer (NK) cells attack cancerous cells. Plasma cells secrete antibodies.

complement proteins work by

forming pores in the membranes of target cells -The term complement system, or simply complement, refers to a group of at least 20 plasma proteins that normally circulate in the blood in an inactive state. These proteins include C1 through C9, factors B, D, and P, plus several regulatory proteins. Complement provides a major mechanism for destroying foreign substances in the body. Its activation unleashes inflammatory chemicals that amplify virtually all aspects of the inflammatory process. Activated complement also lyses and kills certain bacteria and other cell types. (Luckily our own cells are equipped with proteins that normally inhibit complement activation.) Although complement is a nonspecific defensive mechanism, it "complements" (enhances) the effectiveness of both innate and adaptive defenses. The classical pathway involves antibodies, water-soluble protein molecules that the adaptive immune system produces to fight off foreign invaders. When antibodies bind to pathogens, they can also bind complement components. This double binding, called complement fixation, is the first step in this complement activation pathway. The lectin pathway involves lectins, water-soluble protein molecules that the innate immune system produces to recognize foreign invaders. When lectins bind specific sugars on the surface of microorganisms, they can then bind and activate complement. The alternative pathway is triggered when spontaneously activated C3 and other complement factors interact on the surface of microorganisms. These microorganisms lack the complement activation inhibitors our own cells have. Like the blood clotting cascade, complement activation by any of these pathways involves a cascade in which proteins are activated in an orderly sequence—each step catalyzing the next. The three pathways converge at C3, which is split into C3a and C3b. Splitting C3 initiates a common terminal pathway that enhances inflammation, promotes phagocytosis, and can cause cell lysis. Cell lysis begins when C3b binds to the target cell's surface and triggers the insertion of a group of complement proteins called MAC (membrane attack complex) into the cell's membrane. MAC forms and stabilizes a hole in the membrane that allows a massive influx of water, lysing the target cell. The C3b molecules act as opsonins. As previously described, opsonins coat the microorganism, providing "handles" that receptors on macrophages and neutrophils can adhere to. This allows them to engulf the particle more rapidly. C3a and other cleavage products formed during complement fixation amplify the inflammatory response by stimulating mast cells and basophils to release histamine and by attracting neutrophils and other inflammatory cells to the area.

a person may harbor pathogens walled off in __________ for years without displaying any symptoms

granuloma -Some bacteria, such as tuberculosis bacilli, resist digestion by the macrophages that engulf them. They escape the effects of prescription antibiotics by remaining snugly enclosed within their macrophage hosts. In such cases, granulomas form. These tumor like growths contain a central region of infected macrophages surrounded by uninfected macrophages and an outer fibrous capsule. A person may harbor pathogens walled off in granulomas for years without displaying any symptoms. However, if the person's resistance to infection is ever compromised, the bacteria may be activated and break free, leading to clinical disease symptoms.

without __________, an adaptive immune response cannot be initiated

helper t cells -Helper T (TH) cells play a central role in adaptive immunity, mobilizing both its humoral and cellular arms . Once activated by APC presentation of antigen, TH cells help activate B and T cells, and induce B and T cells to proliferate. In fact, without the help of "director" TH cells, there is no adaptive immune response. Their cytokines furnish the chemical help needed to recruit other immune cells. The crucial role of TH cells in immunity is painfully evident when they are destroyed, as in AIDS.

which cells stimulate both arms of the immune response

helper t cells -When activated, CD4 and CD8 cells differentiate into the three major kinds of effector cells of cellular immunity. CD4 cells usually become helper T (TH) cells that help activate B cells, other T cells, and macrophages, and direct the adaptive immune response. CD8 cells become cytotoxic T (TC) cells that destroy cells in the body that harbor anything foreign. Some CD4 cells become regulatory T (TReg) cells, which moderate the immune response. Activated CD4 and CD8 cells can also become memory T cells. Note that the names of the effector cells (helper, cytotoxic, regulatory) are reserved for activated T cells, while naive T cells are simply called CD4 or CD8 cells.

proteins that attach to antigen

immunoglobulins -Antibodies, also called immunoglobulins (Igs), constitute the gamma globulin part of blood proteins. As we mentioned earlier, antibodies are proteins secreted in response to an antigen by effector B cells called plasma cells, and the antibodies bind specifically with that antigen. They are formed in response to an incredible number of different antigens. Despite their variety, all antibodies can be grouped into one of five Ig classes.

when a localized area exhibits increased capillary filtration, hyperemia, and swelling, it is an indication that

inflammation is occurring -Inflammation is triggered whenever body tissues are injuredby physical trauma, intense heat, irritating chemicals, or infection by viruses, fungi, or bacteria. This inflammatory response to injury is summarized in the figure below. Inflammation has several beneficial effects: It prevents the spread of damaging agents to nearby tissues It disposes of cell debris and pathogens. It alerts the adaptive immune system. It sets the stage for repair. The four cardinal signs of short-term, or acute, inflammation are redness, heat (inflam = set on fire), swelling, and pain. Some authorities consider impaired function to be a fifth cardinal sign. For instance, movement in an inflamed joint may be hampered temporarily, forcing it to rest, which aids healing. Although antigens and antibodies may be present and an immune response may be occurring, an area that exhibits increased capillary filtration, hyperemia, and swelling, is a direct indication that inflammation is occurring.

select the enzyme in saliva and lacrimal fluids that destroys bacteria

lysozyme -found in saliva, respiratory mucus, and lacrimal fluid of the eye—destroys bacteria. Protein-digesting enzymes in the stomach kill many different microorganisms. Amylase, trypsin, reverse trascriptase, and pepsin are enzymes with various functions, but are not found in lacrimal secretions, nor do they play a role in destroying bacteria as part of the innate responses.

which of the following is a nonspecific barrier defense

mucous membranes -The innate (nonspecific) defense system, like a lowly foot soldier, is always prepared, responding within minutes to protect the body from foreign substances. This system has two "barricades." The first line of defense is the external body membranes—intact skin and mucosae. The second line of defense, called into action whenever the first line has been penetrated, relies on internal defenses such as antimicrobial proteins, phagocytes, and other cells to inhibit the invaders' spread throughout the body. The hallmark of the second line of defense is inflammation.

which nonspecific defense cells specialize in attacking cancer cells and virus-infected cells

natural killer cells -Natural killer (NK) cells, which "police" the body in blood and lymph, are a unique group of defensive cells that can lyse and kill cancer cells and virus-infected body cells before the adaptive immune system is activated. NK cells are part of a small group of large granular lymphocytes. Unlike lymphocytes of the adaptive immune system, which only recognize and react against specific virus-infected or tumor cells, NK cells are far less picky. They can eliminate a variety of infected or cancerous cells by detecting general abnormalities such as the lack of "self" cell-surface proteins called MHC. The name "natural" killer cells reflects their nonspecificity. NK cells are not phagocytic. They kill by directly contacting the target cell, inducing it to undergo apoptosis (programmed cell death). This is the same method used by cytotoxic T cells. NK cells also secrete potent chemicals that enhance the inflammatory response. Basophils, helper T-cells, macrophages, and plasma cells do not directly attack and destroy cancer and virus-infected cells.

which of the following is not one of the cardinal signs of inflammation

opsonization -The four cardinal signs of short-term, or acute, inflammation are redness, heat (inflam = set on fire), swelling, and pain. Some authorities consider impaired function to be a fifth cardinal sign. For instance, movement in an inflamed joint may be hampered temporarily, forcing it to rest, which aids healing. Opsonization is the process of coating a pathogen with antibodies to aid in clearing it from the body.

immunity gained from injections of clonal antibodies to fight off a current pathogen invasion

passive artificial -Passive immunity can also be conferred artificially by administering exogenous antibodies (from outside your own body) as gamma globulin, harvested from the plasma of an immune donor. Exogenous antibodies are used to prevent hepatitis A and treat poisonous snake bites (antivenom), botulism, rabies, and tetanus (antitoxin) because these rapidly fatal diseases would kill a person before active immunity could be established. The donated antibodies provide immediate protection, but their effect is short-lived (two to three weeks).

immunity gained from transport of antibodies across the placental membrane or through the mother's milk

passive natural -Passive immunity is conferred naturally on a fetus or infant when the mother's antibodies cross the placenta or are ingested with the mother's milk. For several months after birth, the baby is protected from all the antigens to which the mother has been exposed.