Bio 103 Lake Tahoe Community College

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  • 1. Bio 103 Lake Tahoe Community College Winter Quarter Instructor: Sue Kloss __________________________________________________________________________________________________________________________ Chapter 43: The Immune System __________________________________________________________________________________________________________________________ I. Nonspecific Defenses Against Infections A. Nonspecific defenses (innate immunity) vs. infection include skin, mucous membranes, phagocytic cells and antimicrobial proteins 1. Body’s first line of defense against infection are nonspecific (fig. 43.2) a. skin is very important b. Outer layer of intact skin is a tough layer of dead cells, impenetrable to most bacteria & viruses c. acids secreted in sweat and oils on skin (pH from 3 – 5) inhibit many microbes’ growth d. sweat, saliva and tears also have lysozyme - enzyme that attacks cell walls of many bacteria 2. Two organ systems that are inside the body open to the outside guarded by mucous membranes a. digestive system b. respiratory system c. genitourinary 3. other nonspecific defenses as well- stomach acid kills most bacteria we swallow; hepatitis A virus can live 4. nostril hairs filter and trap incoming particles, and 5. mucous membrane in throat, nasal passages and respiratory tubes trap most microbes and dirt that gets past nasal filter. (Fig. 43.3) a. mucus is a viscous fluid that traps microbes and other particles B. Internal cellular defenses 1. microbes that get past all these defenses are confronted by nonspecific defensive cells, all classified as white blood cells 2. These are found in interstitial fluids as well as blood vessels. 3. Neutrophils (60 – 70 % of all white blood cells) and monocytes (5%) are phagocytic white blood cells; they engulf bacteria and viruses in infected tissue. (Fig. 43.4) a. macrophages (“big eaters”) are large phagocytic cells that develop from monocytes. b. macrophages wander in the interstitial fluid, eating any bacteria and virus infected cells they encounter c. neutrophils attach to receptors in cell membrane of pathogens, but not own bodys cells 4. eosinophils have low phagocytic capability, but are effective against parasites like flukes a. they position themselves against invader’s body, then discharge enzymes to destroy it. C. Other nonspecific defenses are antimicrobial proteins that either attack microbes or impede their reproduction 1. when a cell is invaded by a virus, the cell will produce interferons- proteins that help other cells resist viruses 2. interferons diffuse to neighboring cells and induce them to make proteins that inhibit virus reproduction a. these proteins are not virus specific; will work against non related viruses b. resistance is short term and seems to work best vs. flu and cold viruses 3. recombinant DNA technology has made it possible to use large amounts of interferons to fight nasty viral infections and have also been useful in fighting some cancers 4. complement proteins circulate in inactive form in blood plasma; activated by immune system or by microbes. a. Some of these proteins coat the surfaces of microbes, making them easier for the macrophages to engulf. b. other complement proteins cut lethal holes in microbial membranes c. complement proteins amplify other nonspecific defense - inflammatory response C. natural killer cells attack cancer cells and infected body cells, esp. those harboring viruses D. Inflammatory response mobilizes nonspecific defense forces 1. inflammatory response is a major component of nonspecific defense 2. any damage to tissue, whether microbes or injury related, even an insect bite, triggers it 3. mosquito bite: a. skin in bite area becomes red, swollen and warm - inflammation (“setting on fire”) 4. Inflammatory response (Fig. 43.6) a. damaged cells released chemical signals such as histamines 1
  • 2. b. signals cue mobilization of various defenses c. Histamine signals neighboring blood vessels to dilate and become leaky d. blood flow increases to area, plasma passes out of leaky vessels into interstitial fluids of damaged area. e. Other chemicals signal for phagocytes and other white cells, they migrate out of vessels f. results: cleaning and disinfecting injured tissues g. wbc’s engulf bacteria and remains of cells killed by them or physical injury h. Many white cells die in process, their remains are also engulfed and digested I. inflammatory response helps prevent infection spread to neighboring cells j. clotting proteins and platelets leaked into area with plasma seal off infected tissue so healing can begin 5. inflammatory response can be local or systemic a. if microbes get into blood, wbc’s increase b. fever- high body temp that stimulates phagocytes and inhibits microbe growth c. toxins or the wbcs may release compounds to trigger the fever E. The lymphatic system becomes a crucial battleground during infection 1. lymph system is involved in both specific and nonspecific resistance 2. lymphatic system consists of: (Fig. 43.5) a. network of vessels b. lymph nodes (packed with wbcs called lymphocytes) c. thymus d. tonsils e. appendix f. spleen g. bone marrow 3. lymph is similar to interstitial fluids, but carries less O2 and fewer nutrients 4. lymph system functions: a. return fluids to circulatory system b. fight infection 5. 1% of fluids that leave capillary don’t get returned in circulatory system; lymph system returns it 6. lymphatic vessels take up fluid from tissue spaces in the skin 7. fluid enters the lymphatic system by diffusing in to tiny dead end lymph capillaries intermingled among blood capillaries Lymph capillaries converge to form larger and larger lymph vessels 8. 2 large lymphatic veins fuse with veins in the shoulders, called thoracic duct and right lymphatic duct 9. lymphatic vessels resemble veins in that they have valves to prevent backflow and depend on muscle action 10. infection fighting activities of the lymph system occur in the lymph nodes - packed with lymphocytes and macrophages 11. lymph circulates, carrying microbes and sometimes cancer cells. a. macrophages act against them nonspecifically b. lymphocytes may mount a specific immune response 12. When you are fighting infection, your lymph system becomes major battleground 13. lymph nodes become swollen and tender mainly as a result of multiplication of defensive lymphocytes we refer to these as “swollen glands”; they are most obvious in the neck. II. Specific or acquired immunity A. Immune response counters specific invaders 1. If our nonspecific defenses fail to ward off infection, our immune system provides another line of defense. a. phagocytes secrete cytokines – proteins that help activate hlymphocytes and other cells of the immune system. 2. Our immune system recognizes and defends against invading microbes and against cancer cells (our bodies usually identify these as foreign) 3. our immune system acts more efficiently than nonspecific response 4. It can also amplify some nonspecific responses a. inflammation b. histamines, etc. 5. Nonspecific defenses are always ready, but immune response must be cued by presence of a foreign substance, called an antigen. (the bad guy). 6. when immune system detects an antigen, it responds with a. in increase in the number of cells that either attack the invader directly b. cells that produce defensive proteins called antibodies 2
  • 3. c. defensive cells and antibodies produced for that antigen are ineffective against any other foreign substances. 7. antigen = molecule that elicits an immune response (antibody generating) a. the small portion of an antigen that the lymphocytes bind to is called the antigenic determinant, or eptitope. An antigen may have several epitopes. (Fig. 43.7) b. 8. antigens can be certain molecules on surface of viruses, bacteria, mold spores, cancer cells, pollen, house dust, as well as molecules on the cell surfaces of transplanted organs 9. an antibody is a protein found in blood plasma that attaches to one particular kind of antigen on a particular epitope and helps fight its effects 10. immune system has “memory” and can respond quickly to antigens it has encountered before 11. will kill invader organisms before it can produce symptoms, conferring immunity 12. immune system is adaptive, unlike nonspecific defense- exposure to a particular antigen enhances response in future to that antigen 13. immunity = resistance to specific invaders a. acquired by natural infection b. or vaccination - immune system encounters nondisease causing form of antigen to spur defense c. vaccination has be successful in many viral diseases, including polio, smallpox, mumps, measles. We’re trying for an AIDs vaccine but no luck yet 14. active immunity - you produce the antibodies yourself as a result of exposure to disease organism or to a vaccine 15. passive immunity - you get antibodies from someone else who has produced them - e.g. fetus from mom in breast milk, or travel vaccines 16. passive immunity is temporary bc the antibodies you are given only remain effective for a few weeks or months B. Antigen Recognition by Lymphocytes 1. lymphocytes- wbcs that spend most time in tissues and organs of lymphatic system 2. lymphocytes produce the immune response 3. like all blood cells, lymphocytes originate from stem cells in bone marrow 4. some lymphocytes remain in bone marrow and continue to develop = B cells, or B lymphocytes 5. T cells are carried by blood from marrow to thymus gland, near the heart. Both T and B cells eventually make their way via blood to lymph nodes and other lymphatic organs 6. B and T cells work together in defense; they recognize antigens by means of antigen specific receptors embedded in their plasma membrane a. all the receptors on a single cell are identical, all recognize the same epitope b. in other words, each lymphocyte displays specificity for a particular epitope. 7. B cells secrete antibodies which dissolve in the blood and fluids- humoral immunity a. immunity conferred by antibodies 1. composed of proteins very similar to B cell receptors (fig. 43.8) 2. Antigen receptors are made up of Y shaped polypeptides consisting of heavy chains (constant regions) joined by a disulfide bridge, and light chains (variable amino acid sequence for different antigens) b. defends primarily against bacteria and viruses in body fluids by secreting antibodies, or immunoglobulins 1. structurally similar to B cell receptor but lack transmembrane region that anchor receptors in plasma membrane c. antibodies are carried in blood and lymph to infection sites in body d. humoral immunity, or the part of the immune system which is mediated thru the body’s fluids by the B cells, can be transferred for passive immunity thru injections of an immune individual to a nonimmune individual 8. immunity conferred by T cells is cell-mediated immunity a. cannot be passively transferred with plasma b. can only be transferred passively by giving actual T cells from immune to non-immune individual c. T cells circulate in blood and lymph, actively attacking cells w/invaders 1. T cell receptors for an antigen consist of 2 polypeptide chains, alpha and beta, linked by disulfide bridge with C and V regions (Fig. 43.8) 2. V regions have different amino acid sequences to bind to various antigens, or actually small fragments of them, which have been bound to normal cell surface proteins called major histocompatibility complex (MHC) molecules. 3
  • 4. 3. As the T cells make MHC molecules, the molecules bind to fragments of antigens within the cell, and bring it to surface = antigen presentation 4. Nearby T cells can detect antigen’s presence on cells surface 5. How do foreign antigens end up inside T cells? 2 ways. See (Fig. 43.9) a. Class I MHC molecules found in most nucleated cells of body – bind peptides from foreign antigens synthesized in the body; recognized by cytotoxic T cells b. Class II MHC molecules found in phagocytes of the body – recognized by Helper T cells c. each vertebrate spp has multiple alleles for each class I and II MHC gene; these are the most polymorphic genes known d. T cells also work against fungi and protozoans and are thought to be important in protecting body from its own cancerous cells e. T cells also promote phagocytosis in other wbcs f. T cells stimulate B cells to produce antibodies g. T cells are therefore involved in both humoral and cell mediated immunity 9. When a T cell develops in thymus or B cell develops in bone marrow, genes in those cells are turned on and cell synthesizes molecules of a specific protein and builds them into a plasma membrane 10. These protein molecules stick out from the cell surface (Fig. 24.5 - dark purple structures) 11. These molecules are called antigen receptors - bind to a specific antigen 12. Once a B or T cell has it surface proteins in place it can recognize a specific antigen and go after it 13. Once the B or T cell have antigen receptors, they go via blood to lymph nodes, spleen, or other parts of lymph system; they hang out there and wait 14. when they encounter an antigen they are programmed to recognize, they differentiate further and become a fully mature component of the immune system 15. Enormous diversity of T and B cells. Estimates of 100 billion different kinds - enough to recognize and bind to virtually any antigen we would ever encounter 16. A small population of each kind lie in wait in our immune system, genetically programmed to respond to different antigens 17. Antigenic determinants - localized regions on the surface of the antigen molecule 18. whole organism or cell is NOT the antigen, just the surface molecule that cues immune response C. Generation of lymphocyte diversity by Gene Rearrangement in B cells 1. Secquence of amino acids in a V part of the chain determines the epitope the antibody can bind to 2. an enzyme called recombinase randomly joins one variable (V) gene segment to one of the 5 Joining (J) segments (Fig. 43.11) a. it can link any of 40 V segments to any of 5 J segments, so there are 200 possible gene products 3. this constitutes the light chain portion of the protein molecules and occurs early in B cell development 4. once the V-J rearrangement is complete, transcription and translation can occur D. Testing and removal 1. since rearrangement of the antigen receptors is random, it is possible that antigen receptors are specific for the body’s own molecules 2. As B and T cells mature in the bone marrow and Thymus, respectively, their antigen receptors are tested for potentioal self reactivity 3. for example, developing T cells are tested against class I and class II MHC molecules, which are both expressed at high levels in the thymus 4. lymphocytes bearing receptors specific for your bodys molecules are either destroyed by apoptosis or rendered nonfunctional, leaving only lymphocytes that react wtih nonself molecules 5. thus the immune system exhibits the critical feature of self tolerance 6. failure of self tolerance can lead to autoimmune diseases such as multiple sclerosis E. Clonal selection of lymphocytes 1. soluble antigens or antigens present on surface of microbe, infected body cell or cancer cell encounters a large array of B and T cells in body 2. however, only a few lymphocytes bearing receptros specific for epitopes on that antigen interact with it 3. selection of B cell or T cell by an antigen activates the lymphocyte, stimulating it to divide many times and differentiate into two types (clones) of daughter cells (fig 43.12) a. effector cells are produced in large numbers, and are short lived 1. effector cells act differently depending on whether they are B cells 2. helper T cells or 3. cytotoxic T cells b. memory cells - long lived cells bearing receptors specific for the same inducing antigen 4. AGAIN - CLONAL SELECTION IS: EACH ANTIGEN BINDS TO SPECIFEC RECEPTORS, 4
  • 5. SELECTIVELY ACTIVATES A TINYFRACTION OF THE BODY’S DIVERSE POOL OF LYMPHOCYTES. THIS RELATIVELY SMALL NUMBER OF SELECTED CELLS GIVES RISE TO CLONES OF THOUSANDS OF CELLS, ALL SPECIFIC FOR AND DEDICATED TO ELIMINATING THAT ANTIGEN 5. primary immune response - selective proliferation and differentiation of lymphocytes that occurs the first time a body is exposed to a particular antigen (Fig. 43.13) a. max dffector response does not occur until about 10 to 17 days after exposure to antigen b. during this time, selected B cells generate antibody- secreting efffector b cells called plasma cells c. T cells are activated to various effector forms (coming up in discussion) d. while these cells are developing, a stricken individual may become ill e. individual recovers as T and B cells clear antigen from body 6. secondary immune response - if individual is exposed again to the same antigen, response is a. faster (2 - 7 days) b. more prolonged and c. of greater magnitude 7. immune systems capac ity to generate secondary immune response is called immunological memory a. depends on clones of long lived T and B memory cells generated following exposure to the antigen initially b. memory cells - last for decades, remain in the lymph nodes, ready to be activated c. sometimes seem to confer lifetime immunity, eg. measles and mumps III. B Cells confer Humoral Immunity and T cells confer cell mediated immunity A. intro 1. Humoral immunity - B cells secrete antibodies that circulate in the blood and lymph and bind to antigens a. body fluids used to be called humors 2. cell mediated immune response - activation aond clonal selection of cytotoxic T cells which directly destroy target cells (Fig. 43.14) 3. Helper T is central to this process a. Helper Ts respond to peptide antigens displayed on antigen presenting cells and in turn stimulate activation of nearby cytotoxic Ts and B cells B. Helper T cells: a response to nearly all antigens 1. when a helper T cell encounters and recognizes a class II MHC molecule- antigen comolex on an antigen presenting cell, the helper T proliferates and differentiates into a clone of activated helper T cells and memory helper T cells 2. helper Ts have a surface protein called CD4 that binds to the class II MHC molecule to keep these cells joined while activation proceeds 3. activated helper Ts secrete cytokines that stimulate other lymphocytes a. promotes cell mediated and humoral response 4. Class II MHC molecules recognized by helper Ts are found mainly on macrophages and B cells, and another important immune system cell called dendritic cells a. dendritic cells are effective at presenting antigens to naive helper Ts - first exposure b. in other words, dendritic cells particularly important in triggering primary immune response c. dendritic cells reside in skin and other tissues where they effectively capture antigens d. they then migrate to lymphoid tissues where they present antigens via class II MHC molecules to helper Ts (Fig. 43.15) e. macrophages present antigens to memory helper Ts f. B cells present antigens to helper Ts in humoral immunity C. Cytotoxic T Cells - response to infected cells and cancer cells 1. cytotoxic Ts- effectors of cell mediated immunity a. eliminate body cells infected by viruses or other intracellular pathogens as well as cancer cells and transplanted cells b. fragments of nonself proteins synthesized in target cells accociate with class I mMHC molecules and are displayed on cell surface c. there they can be recognized by cytotoxic Ts 1. surface protein called CD8 helps bind cytotoxic T to target 2. similar to interactions of CD4 and class I MHC molecules but in different cell types d. this activates the cyto T to differentiate into an active killer e. cytokines secreted from nearby helper Ts promote this activation f. activated cyto T secretes protesins that act on the bound infected cell, leading to destruction (Fig. 43.16) - perforin and granzymes (proteolytic enzymes) g. death of infected cell exposes pathogen to circulating antibodies, which mark it for disposal h. the cyto T moves on to destroy other infected cells with same pathogen 5
  • 6. 2. Tumor cells carry tumor antigens not found on normal body cells a. allow immune system to identify them as foreign b. Class I MHC molecules in cells present fragments of tumor antigens to cyto Ts c. certain cancers and viruses (Epstein Barr) actively reduce class I MHC molecules on affected cells, heping them escape detection by cyto Ts d. Natural Killer cells can induce apoptosis in virus infected and cancer cells D. B Cells - response to extracellular pathogens 1. antigens that elicit immune response are typically proteins and polysaccharides present on bacteria surface a. allergens can also elicit humoral response, inappropriately 2. B cells are stimulated both by antigen and by helper Ts responding to same antigen, which release cytokines 3. B cell proliferates into a clone of antibody secreting plasma cells and a clone of memory B cells 4. When antigen binds to B cell, it takes in some of the antigen (fig. 43.17) a. B cell presents antigens to helper T cell b. this type of direct cell to cell contact is critical to activation of the B cells c. unlike macrophages and dendritic cells, a B cell can only present the antigen to which it binds 5. Most antigens recognized by B cells contain multiple epitopes, so that exposure to one antigen can stimulate a variety of different B cells, each giving rise to a cloneof thousands of plasma cells 6. all plasma cells in one clone produce antibodies specifically for that epitope only 7. each plasma cell secretes ~2000 antibodies /sec for the cell’s 4-5 day life span E. Antibody mediated disposal of antigens 1. (Fig. 43.19) Main role of antibodies in eliminating invading microbes is to mark the invaders a. mark = binding so that antibody-antigen complex is formed b. weak chemical bonds hold the complex together c. it is the binding that triggers mechanisms to neutralize or destroy an invader d. mechanism is called an effector mechanism e. there are a number of different mechanisms your defense system can employ 1. neutralization - binding of antibody to antigen physically blocks harmful antigens making them ineffective - (block attachment surface molecules of antigen, so it cant attach; or they may bind to toxin molecules on bacteria); Phagocytes like macrophages then dispose of the complexes 2. agglutination - clumping invading organisms together; each antibody has at least 2 binding sites to accomplish this; phagocytes can then catch them 3. precipitation - link dissolved antigen molecules together, so they precipitate out of solution as solids. Easy for phagocytes to engulf. 4. activation of complement proteins - one of the most important effector mechanisms) activated complement proteins (green in the diagram) can attach to foreign cells and open holes in cell membrane (lysine) 1. B cells are the primary defenders in humoral immunity 2. primary response of humoral immunity - (initial encounter with antigen) a. surface receptors (specific antibodies) on B cell bind with antigen molecules (antigenic determinants). b. binding triggers growth, division and differentiation of that B cell c. resulting clone contains many effector B cells, the guys who will actually fight, (plasma cells) d. and memory B cells e. Since the plasma cells actually secrete the antibodies, they are the true front line defenders f. they may secrete 2000 antibodies/sec for their 2 or 3 day lifetime g. antibodies circulate in the blood and lymph h. primary response ends as the plasma cells die out 3, secondary response of humoral immunity - a. memory cells are the subs in the game b. await future exposure to antigens 6
  • 7. c. may occur years later d. memory cells bind to antigens and are stimulated to produce large new clones of cells e. it occurs more rapidly and yields more plasma cells than initial response f. antibody levels in blood and lymph are much higher than in the primary response 4. Main role of antibodies in eliminating invading microbes is to mark the invaders a. mark = binding so that antibody-antigen complex is formed b. weak chemical bonds hold the complex together c. it is the binding that triggers mechanisms to neutralize or destroy an invader d. mechanism is called an effector mechanism e. there are a number of different mechanisms your defense system can employ 1. neutralization - binding of antibody to antigen physically blocks harmful antigens making them ineffective - (block attachment surface molecules of antigen, so it cant attach; or they may bind to toxin molecules on bacteria); Phagocytes like macrophages then dispose of the complexes 2. agglutination - clumping invading organisms together; each antibody has at least 2 binding sites to accomplish this; phagocytes can then catch them 3. precipitation - link dissolved antigen molecules together, so they precipitate out of solution as solids. Easy for phagocytes to engulf. 4. activation of complement proteins - one of the most important effector mechanisms) activated complement proteins (green in the diagram) can attach to foreign cells and open holes in cell membrane (lysine) E. T cells mount cell mediated defense and aid humoral immunity 1. B cells work against invaders in the blood, interstitial fluids and lymph 2. many invaders, including viruses, enter cells and reproduce there. 3. Cell mediated immunity (T cells) battles pathogens inside body cells 4. T cells respond only to antigens present on the surfaces of the body’s own cells 5. 2 kinds of T cells a. cytotoxic T cells b. helper T cells 6. Helper T cells have many roles in immunity a. activate cytotoxic T cells b. activate macrophages c. stimulate B cells to produce antibodies 7. Helper Ts interact with other wbcs that become antigen- presenting cells (APCs) a. all of cell mediated immunity and much humoral immunity depends on interaction of APCs and Helper T’s. b. this interaction serves to activate the Helper Ts. c, APC presents a foreign antigen to a Helper T. d. a typical APC is a macrophage (Fig. 21.13) 1. macrophage ingests and breaks apart a pathogen 2. self proteins (belong to our bodies, not pathogens) will bind to antigen (nonself) 3. APC will display self-nonself complex on the surface of the cell 4. each of us has a unique set of self proteins, used as unique markers, which is what keeps your body from destroying itself, unless you have autoimmune disease 5. Helper Ts recognize and bind to the COMBINATION of the self and antigen molecules. This double recognition system is like the system you always see in movies about nukes - two keys, used in unison, are required for launch 6. Ability to recognize a unique self-nonself complex on an APC depends on T cell receptors (purple structures) embedded in plasma membrane 7. T cell receptors have 2 binding sites - one for self proteins, one for antigen 8. this allow T cell to recognize self-nonself complex on an APC 7
  • 8. 9. highly specific - each Helper T can bind only to one kind of self-nonself complex on APC 10. binding activates the helper T; diffusion of certain chemical signals (interleukin-1) stimulate the Helper T. 11. Helper T will then promote immune response a. secretion of several stimulatory proteins b. example of stimulatory protein = interleukin-2 has 3 major effects 1) makes Helper T grow and divide to produce memory and additional Helper Ts. Positive feedback loop amplifies cell mediated defense 2) stimulates activity of Cytotoxic T cells 3) activates B cells, stimulating humoral immunity 12. Cytotoxic T cells are the only T cells that actually kill other cells 13. infected body cells are important targets 14. Infected cells have foreign antigens attached to self proteins on coats (Fig. 24.13C) 15. Like Helper Ts, Cytotoxic Ts have receptors (purple) that bind w/ self-nonself complex 16. Self-nonself complex on infected cell is redflag to Cytotoxic T’s with matching receptors 17. binding initiates chemical signal pathway that activates the T cell 18. activated T cell synthesizes a protein called perforin 19. perforin attaches to infected cell membrane, putting holes in it. Infected cell dies. F. Cytotoxic T cells may help prevent cancer 1. people with immune deficiencies are unusually prone to cancer, suggesting that the immune system plays role in preventing cancer. 2. Some changes that take place on the outside of a cell due to cancer; this helps ummune system identify the cancer cells as foreign. Fig. 24.12. 3. Our immune system has self proteins on cell surfaces to allow our immune system to attack invading cells without attacking our own cells. Our lymphocytes do not attack cells that have self proteins. 4. this may be a disadvantage at times, for example during organ transplants. a. preventing transplant rejection - use monoclonal antibodies to target and destroy T cells that attack the transplant b. use stem cells to establish new immune system that recognizes the transplant. F. Malfunction of failure of immune system can cause disease. 1. autoimmmune diseases - immune system turns against the body’s own molecules. a. lupus - B cells make antibodies against many sorts of molecules, even histones and and DNA released by normal breakdown of body cells. b. rheumatoid arthritis results in damage and painful inflammation of cartilage and bone of joints. c. diabetes - insulin producing cells of the pancreas are destroyed d. in MS, T cells react against myelin 1. immunodeficiency disease - lack one or more components of normal immune system. a. radiation therapy often causes this, as does HIV and Hodgekins disease a type of cancer that affects the lymphocytes 1. Physical and emotional stress may also weaken the immune system 2. Allergies are overreactions to environmental antigens - abnormal sensitivities to antigens in surroundings a. antigens that cause allergies are called allergens 1. proteins on pollen grains 2. proteins on dust mites and in animal dander 8
  • 9. ch 43 1. Explain what is meant by nonspecific defense and list the nonspecific lines of defense in the vertebrate body. 2. Distinguish between: a. innate and acquired immunity b. humoral and cell mediated response 3. Explain how the physical barrier of skin is reinforced by chemical defenses. 4. Define phagocytosis. Name four types of phagocytic leukocytes. 5. Explain how interferon limits cell-to-cell spread of viruses. 6. Describe the inflammation response, including how it is triggered. 7. Describe the factors that influence phagocytosis during the inflammation response. 8. Explain how the action of natural killer cells differs from the action of phagocytes. 9. Explain what occurs during the condition known as septic shock. 10. Describe the roles of antimicrobial proteins in innate immunity. 11. Distinguish between antigens and antibodies. 12. Distinguish between antigen and epitope. 13. Explain how B lymphocytes and T lymphocytes recognize specific antigens 14. Explain how the particular structure of a lymphocyte’s antigen binding site forms during development. Explain the role of recombinase in generating the staggering variability of lymphocytes. 15. Explain why the antigen receptors of lymphocytes are tested for self-reactivity during development. Predict the consequences that would occur if such testing did not take place. 16. Describe the mechanism of clonal selection. Distinguish between effector cells and memory cells. 17. Distinguish between primary and secondary immune responses. 18. Describe the cellular basis for immunological memory. 20. Compare the structures and functions of cytotoxic T cells and helper T cells. 21. Compare the production and functions of class I MHC and class II MHC molecules. 22. Distinguish between humoral immunity and cell-mediated immunity. 23. Describe the roles of helper T lymphocytes in both humoral and cell-mediated immunity. 24. Describe the functions of the proteins CD4 and CD8. 25. Explain how cytotoxic T cells and natural killer cells defend against tumors. 27. Explain why macrophages are regarded as the main antigen-presenting cells in the primary response but memory B cells are the main antigen-presenting cells in the secondary response. 28. Explain how antibodies interact with antigens. 29. Diagram and label the structure of an antibody and explain how this structure allows antibodies to (a) recognize and bind to antigens, and (b) assist in the destruction and elimination of antigens. 30. Distinguish between the variable (V) and constant (C) regions of an antibody molecule. 31. Describe the production and uses of monoclonal antibodies. 32. Compare the processes of neutralization, opsonization, and agglutination. Describe the importance of, and how complement proteins work in destroying affected cells. 33. Distinguish between active and passive immunity and describe examples of each. 34. Describe the infectious agent that causes AIDS and explain how it enters a susceptible cell. 35. Explain how HIV is transmitted and describe its incidence throughout the world. Note strategies that can reduce a person’s risk of infection. 9