Immune System

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  • From: http://www.postgradmed.com/issues/1997/06_97/vetter.htm, accessed 8/31/04.
  • from: http://images.google.com/imgres?imgurl=http://203.65.72.83/en/dpc/Upload/wpe63.jpg&imgrefurl=http://www.cdc.gov.tw/en/dpc/ShowPublication.ASP%3FRecNo%3D709&h=200&w=141&sz=12&tbnid=O5tJ7B2XcdEJ:&tbnh=97&tbnw=69&start=111&prev=/images%3Fq%3Delephantiasis%26start%3D100%26hl%3Den%26lr%3D%26ie%3DUTF-8%26sa%3DN “ Prior to the 1970's residents in Taiwan's coastal areas and in the outlying island groups of Penghu (Pescadores), Kimen and Matsu commonly suffered from filaria parasite infection, or "filariasis." Although the filariasis death rate is not high, the filaria parasite causes obstruction of lymph circulation and unsightly swelling in diverse parts of the body, occasioning pain as well as shame at one's appearance, and seriously effecting filariasis victims' general quality of life. Thanks to the concerted efforts of a special filariasis eradication task force and public health agencies, the original rates of infection in those regions -- as high as 20% -- were reduced to zero within a short time, making Taiwan the world's first country to totally eradicate the disease. “ Filariasis pathology “ Filariasis is an infectious disease caused by the filaria parasite, a nematode worm, which is transmitted to humans via mosquito vectors and which, in its adult stage of development, resides in the lymphatic system. In all, there are 7 known types of filaria in the world, four of which can infect humans. Two of these latter four filariae, Wuchereria bancrofti and Brugia Malayi , are found in Southeast Asia and Taiwan. “
  • Picture is of cow intestines.
  • Classic example of how accute inflammation differs histologically from chronic inflammation. In acute, you will see granulolcytes rush to the area such as in the photo. Chronic inflammation will instead house many lymphocytes (agranulocytes) such as plasma cells and T cells. Caption for photo: Section of an inflamed intestinal lamina propria. Inflammation was caused by nematode parasitism. Aggregated eosinophils and plasma cells function mainly in the connective tissue by modulating the inflammatory process. Giemsa stain. Low magnification.
  • Go to Paul Kubes’ website (U of Calgary) for great online video of MARGINATION neutrophils rolling and tethering to endothelium just prior to diapedesis. It is an awesome video!!!!! Within minutes, monocytes and neutrophils respond to site of infection. Photo caption (from Paul Kubes’ website): Leuckocyte recruitment in a healthy(A) and diseased (B) brain. No leukocyte recruitment is observed in the post-capillary venules in the healthy brain. In contrast, many leukocytes can be seen rolling and adhering in the diseased brain. The yellow SEM photo shows a leukocyte (probably a macrophage) phagocytosing bacteria.
  • SEM Photo: Human T-lymphocyte Attacking Fibroblast Tumor / Cancer Cells.
  • From: http://www.medscape.com/viewarticle/405806_print Picture is of a man with anti-convulsant (drug) hypersensitivity syndrome; second picture shows high eosinophilic count in bone marrow as a result of syndrome ( Figure 4. Bone marrow biopsy, remarkable for reactive hypercellularity (50%-60%), marked eosinophilia, and lobulated, cleft atypical lymphocytes (pseudo-Sézary cells) (hematoxylin and eosin, 200x). “ Discussion AHS is uncommon, occurring in 1 in 1,000 to 1 in 10,000 patients, and is more frequently observed in African-Americans. [5,6] Some investigators suspect that the incidence is underestimated as a result of quantification based on using a denominator combining all antiepileptic drug users rather than new users only. These investigators report that among new users of antiepileptic drugs, there was an incidence of greater than 4 in 10,000 for patients taking phenytoin and carbamazepine, and no reactions among 1,504 patients taking valproic acid. [7] The addition or substitution of antiepileptic drugs should be influenced by the 80% cross-sensitivity between phenytoin, phenobarbital, and carbamazepine; these drugs should not be combined or substituted. [6] First-degree familial association of AHS has been documented. [5] Immediate family members of an affected patient should be prescribed antiepileptic medications only after specific counseling and precautions have been given.”
  • Type I: Cause systemic histamine release; vasodilation, increased capillary permeability; edema, mucus, congestion, watery eyes, runny nose, hives, etc. Type II: Then complement fixation and cytolysis; macrophages then phagocytocize
  • Picture is of poison ivy (type IV) reaction.
  • Immune System

    1. 1. The Lymphatic System and Our immune response: Did you know? <ul><li>Laughing lowers levels of stress hormones and strengthens the immune system. Six-year-olds laugh an average of 300 times a day. Adults only laugh 15 to 100 times a day. </li></ul><ul><li>3000 BC The ancient Egyptians recognize the relationship between exposure to disease and immunity. </li></ul><ul><li>1500 BC The Turks introduce a form of vaccination called variolation, inducing a mild illness that protects against more serious disease. </li></ul><ul><li>1720 Lady Mary Wortley Montagu promotes the variolation principle, launching a campaign to inoculate the English against smallpox. </li></ul><ul><li>A macrophage can consume as many as 100 bacteria before undergoing apoptosis. </li></ul>
    2. 2. What does the lymphatic system do? <ul><li>Return interstitial fluid </li></ul><ul><ul><li>Capillaries only reabsorb 15% </li></ul></ul><ul><ul><li>Funneled into subclavian veins </li></ul></ul><ul><li>Absorb and transport lipids from intestines </li></ul><ul><li>Generate and monitor immune responses </li></ul><ul><li>lymphatic system movie </li></ul>
    3. 3. What is in the lymphatic system? <ul><li>Lacteals and lymphatic capillaries </li></ul><ul><ul><li>Overlapping epithelial cells </li></ul></ul><ul><li>Lymph vessels and ducts </li></ul><ul><ul><li>What happens if blockage occurs? </li></ul></ul><ul><ul><ul><li>See next slide! </li></ul></ul></ul>
    4. 5. What is in the lymphatic system? <ul><li>Lymphatic trunks </li></ul><ul><ul><li>Lumbar, brachiomediastinal, intestinal, jugular, subclavian, intercostal </li></ul></ul><ul><li>R lymphatic duct: R arm, R thorax, R head </li></ul><ul><li>Thoracic duct: everything else </li></ul>
    5. 6. What is in the lymphatic system? <ul><li>Red bone marrow </li></ul><ul><ul><li>Hemopoiesis: what types of leukocytes are manufactured here? </li></ul></ul><ul><li>Mucosa-associated lymphatic tissue </li></ul><ul><ul><li>Sprinkling of lymphocytes in mucosa membranes </li></ul></ul><ul><ul><ul><li>Peyer’s patch : small intestine nodules of lymphatic tissue </li></ul></ul></ul>
    6. 7. What is in the lymphatic system? <ul><li>Thymus </li></ul><ul><ul><li>Secretes thymopoietin for T-cell development </li></ul></ul><ul><ul><li>T-cells mature here </li></ul></ul><ul><ul><li>Thymus atrophies with age </li></ul></ul><ul><li>Tonsils </li></ul><ul><ul><li>Palatine (2), lingual (2), pharyngeal (1; adenoid) </li></ul></ul><ul><ul><ul><li>Tonsillectomy: remove palatines </li></ul></ul></ul><ul><ul><li>Gather, remove and “learn” pathogens from food/air </li></ul></ul><ul><ul><ul><li>Calculate risk in childhood: inviting invasion </li></ul></ul></ul><ul><ul><ul><ul><li>Payoff: greater immunocompentency later in life </li></ul></ul></ul></ul>
    7. 8. What is in the lymphatic system? <ul><li>Lymph nodes </li></ul><ul><ul><li>Filters lymph fluid for antigens, bacteria, etc. </li></ul></ul><ul><ul><ul><li>B-lymphocytes made here </li></ul></ul></ul><ul><ul><ul><li>Some T-lymphocytes and macrophages congregate </li></ul></ul></ul><ul><ul><ul><li>Afferent (more) and efferent (less) vessels </li></ul></ul></ul><ul><ul><ul><ul><li>lymph fluid exits through hilum </li></ul></ul></ul></ul><ul><ul><li>Common site for cancer—Why? </li></ul></ul><ul><ul><ul><li>Hodgkin’s lymphoma: lymph node malignancy </li></ul></ul></ul><ul><ul><ul><ul><li>Etiology unknown </li></ul></ul></ul></ul><ul><ul><ul><li>Non-Hodgkin’s lymphoma: all other cancers of lymphoid tissue </li></ul></ul></ul><ul><ul><ul><ul><li>Multiplication/metastasis of lymphocytes </li></ul></ul></ul></ul><ul><ul><ul><ul><li>5th most common cancer </li></ul></ul></ul></ul>
    8. 9. What is in the lymphatic system? <ul><li>Spleen : dense sieve of reticular CT </li></ul><ul><ul><li>Function s </li></ul></ul><ul><ul><ul><li>Erythropoiesis in fetus </li></ul></ul></ul><ul><ul><ul><li>Stores platelets </li></ul></ul></ul><ul><ul><ul><li>Salvages and stores RBCs parts for recycling (RBC graveyard) </li></ul></ul></ul><ul><ul><li>Red pulp </li></ul></ul><ul><ul><ul><li>Dispose of damaged/dead RBCs and pathogens </li></ul></ul></ul><ul><ul><ul><li>Old RBCs aren’t flexible enough to get through sieve </li></ul></ul></ul><ul><ul><li>White pulp </li></ul></ul><ul><ul><ul><li>Lymphocytes and macrophages </li></ul></ul></ul><ul><ul><ul><li>B-cells proliferate here </li></ul></ul></ul><ul><ul><li>If splenectomy: liver and marrow take over duties </li></ul></ul>
    9. 10. The lymphatic ducts empty directly into the <ul><li>A. Heart </li></ul><ul><li>B. Subclavian veins </li></ul><ul><li>C. Thoracic veins </li></ul><ul><li>D. Brachiocephalic veins </li></ul>
    10. 11. An efferent lymphatic vessel is carrying fluid <ul><li>A. Away from the heart </li></ul><ul><li>B. Towards the lymph node </li></ul><ul><li>C. Out of an area </li></ul><ul><li>D. Away from a node </li></ul>
    11. 12. Which area is not drained by the thoracic duct? <ul><li>A. Right leg </li></ul><ul><li>B. Left leg </li></ul><ul><li>C. Right arm </li></ul><ul><li>D. Left arm </li></ul>
    12. 13. The immune system
    13. 14. What strategies does the immune system use? <ul><li>Non-specific immunity </li></ul><ul><ul><li>Responds without caring about specific type of threat </li></ul></ul><ul><li>Specific immunity </li></ul><ul><ul><li>Tailored to specific pathogens; based on memory </li></ul></ul><ul><ul><li>Two types </li></ul></ul><ul><ul><ul><li>Antibody-mediated immunity (humoral response) </li></ul></ul></ul><ul><ul><ul><li>Cell-mediated immunity </li></ul></ul></ul>
    14. 15. What’s behind non-specific immunity? <ul><li>External barriers </li></ul><ul><ul><li>Skin </li></ul></ul><ul><ul><ul><li>Keratin is tough to penetrate </li></ul></ul></ul><ul><ul><ul><li>Low pH (lactic acid), very dry, nutrient-poor </li></ul></ul></ul><ul><ul><ul><li>Anti-microbial proteins: defensins from neutrophils </li></ul></ul></ul><ul><ul><li>Mucus </li></ul></ul><ul><ul><ul><li>Urine, saliva, tears and mucus </li></ul></ul></ul><ul><ul><ul><li>Contain lysozyme (dissolves peptidoglycan wall) </li></ul></ul></ul><ul><ul><li>Viscous areolar CT matrix </li></ul></ul>
    15. 16. What’s behind non-specific immunity? <ul><li>Phagocytes </li></ul><ul><ul><li>Macrophages : tissue-living monocytes </li></ul></ul><ul><ul><li>Neutrophils : digestion and killing zone (H 2 O 2 ; superoxide ion and hypochlorite (bleach)) </li></ul></ul><ul><ul><li>Eosinophils : less avid digesters </li></ul></ul><ul><ul><li>Basophils and mast cells : it mobilize other WBCs (via histamine and heparin) </li></ul></ul><ul><ul><ul><li>some phagocytosis </li></ul></ul></ul><ul><ul><li>Natural Killer cells (NK cells): type of T-cell </li></ul></ul><ul><ul><ul><li>Only attack infected or cancerous host cells </li></ul></ul></ul>
    16. 17. What’s behind non-specific immunity? <ul><li>Inflammation </li></ul><ul><ul><li>Redness, swelling, heat, pain </li></ul></ul><ul><ul><ul><li>Bradykinin: pain stimuli from mast cells </li></ul></ul></ul><ul><ul><ul><li>Histamine: what two things does it do? </li></ul></ul></ul><ul><ul><li>Leukocyte migration </li></ul></ul><ul><ul><ul><li>Margination </li></ul></ul></ul><ul><ul><ul><ul><li>http://www.med.ucalgary.ca/webs/kubeslab/home/ </li></ul></ul></ul></ul><ul><ul><ul><li>Diapedesis: http://www.constantinestudios.com/animation4.html </li></ul></ul></ul><ul><ul><ul><li>Chemotaxis </li></ul></ul></ul><ul><ul><ul><li>Phagocytosis </li></ul></ul></ul>
    17. 18. What’s behind non-specific immunity? <ul><li>Interferons </li></ul><ul><ul><li>Virus-infected cells secrete warning ( click here or on movie to right ) </li></ul></ul><ul><ul><li>Can promote cancer cell destruction </li></ul></ul><ul><li>Complement proteins </li></ul><ul><ul><li>20+ beta-globulins which perforate bacterial cells (cytolysis) </li></ul></ul><ul><ul><li>complement movie </li></ul></ul><ul><li>Fever (pyrexia) </li></ul><ul><ul><li>Promotes interferon activity </li></ul></ul><ul><ul><li>Elevates BMR </li></ul></ul><ul><ul><li>Discourages bacteria/viral reproduction </li></ul></ul><ul><ul><li>fever movie </li></ul></ul>
    18. 19. The following are symptoms of inflammation EXCEPT <ul><li>A. Edema </li></ul><ul><li>B. Hyperemia </li></ul><ul><li>C. Exudate (pus) </li></ul><ul><li>D. Dehydration </li></ul>
    19. 20. What is specific immunity? <ul><li>Specific response </li></ul><ul><li>Memory for future reinvasion </li></ul><ul><li>Antibody-based </li></ul><ul><ul><li>B cells primary (but not only) actors </li></ul></ul><ul><li>Cell-mediated </li></ul><ul><ul><li>T cells only </li></ul></ul>
    20. 21. What are antibodies? <ul><li>Antibody: gamma globulin (protein) which complexes with a specific antigen </li></ul><ul><ul><li>AKA Immunoglobin (Ig) </li></ul></ul><ul><li>Antigen (Ag): any molecule which causes an immune response </li></ul><ul><ul><li>Not necessarily always dangerous antigen </li></ul></ul><ul><ul><li>Epitopes: different regions where different antibodies bind </li></ul></ul><ul><ul><li>Haptens: too small on their own but can bind with host molecules and cause immune response </li></ul></ul><ul><ul><ul><li>Detergent, poison ivy, penicillin </li></ul></ul></ul>
    21. 22. What do antibodies look like? <ul><li>Protein with quaternary structure </li></ul><ul><ul><li>Two light chains, two heavy chains </li></ul></ul><ul><ul><li>Each chain has variable region </li></ul></ul><ul><ul><ul><li>Combine to form antigen-binding site </li></ul></ul></ul><ul><ul><li>Remainder of chains = constant region </li></ul></ul>
    22. 23. What are the five antibody classes? <ul><li>IgA : prevents pathogens from sticking to epithelia </li></ul><ul><ul><li>Can form dimers </li></ul></ul><ul><li>IgD : antigen receptor in B-cell PM </li></ul><ul><li>IgE : stimulates basophils/mast cells </li></ul><ul><ul><li>Secrete histamines, also causes allergic response </li></ul></ul><ul><li>IgG : most common antibody (75-85%) </li></ul><ul><ul><li>Primary Ig of secondary immune response </li></ul></ul><ul><li>IgM : antigen receptor in B-cell PM </li></ul><ul><ul><li>Can form pentamers </li></ul></ul><ul><ul><li>Predominant Ig of primary immune response </li></ul></ul><ul><ul><li>Includes anti-A and Anti-B of ABO blood groups </li></ul></ul>
    23. 24. How many different antibodies are there? <ul><li>> 2M </li></ul><ul><li>But we only have ~30,000 genes (not 100,000) </li></ul><ul><ul><li>Central dogma (one gene = one protein) doesn’t appear to apply </li></ul></ul><ul><li>Somatic recombination creates variety </li></ul><ul><ul><li>Shuffling of V and J segments </li></ul></ul><ul><ul><li>http://www.cat.cc.md.us/courses/bio141/lecguide/unit3/humoral/antibodies/abydiversity/vdj.html </li></ul></ul>
    24. 25. Which of the following could not be antigenic on its own? <ul><li>A. Protein </li></ul><ul><li>B. Polysaccharides </li></ul><ul><li>C. Haptens </li></ul><ul><li>D. Glycolipids </li></ul>
    25. 26. Antibodies are defense substances produced by the ___ cells. <ul><li>A. T-lymphocytes </li></ul><ul><li>B. Monocytes </li></ul><ul><li>C. B-Lymphocytes </li></ul><ul><li>D. Leukocytes </li></ul>
    26. 27. What are T cells? <ul><li>Migrate from marrow and develop in thymus </li></ul><ul><ul><li>Have antigen receptors on PM = immunocompetent </li></ul></ul><ul><ul><ul><li>Mitosis produces clones </li></ul></ul></ul><ul><ul><li>Clonal deletion destroys self-reactive clones </li></ul></ul><ul><li>Good at destroying cells and stimulating B cells </li></ul><ul><ul><li>They do NOT secrete antibodies as B cells do </li></ul></ul><ul><ul><li>T cell types movie </li></ul></ul>
    27. 28. What are B cells? <ul><li>From marrow: colonize lymph tissues, organs when mature </li></ul><ul><ul><li>Developing B cells synthesize PM antibody </li></ul></ul><ul><ul><ul><li>Each cell has a different antibody covering it </li></ul></ul></ul><ul><ul><li>Mitosis: immunocompetent clones </li></ul></ul><ul><ul><li>One B cell responds to only one antigen </li></ul></ul><ul><li>Serve as antigen-presenting cells (APC) </li></ul><ul><ul><li>So do macrophages </li></ul></ul><ul><ul><li>Lets T cells “see” the antigen </li></ul></ul><ul><li>Secrete antibodies into blood, but do NOT kill cells as T cells do </li></ul><ul><li>B cell types movie </li></ul>
    28. 29. Cell-mediated immunity is mainly a function of <ul><li>A. B cells </li></ul><ul><li>B. T cells </li></ul><ul><li>C. Macrophages </li></ul><ul><li>D. Neutrophils </li></ul>
    29. 30. What happens in a cell-mediated response? <ul><li>The key players: </li></ul><ul><ul><li>Antigen-presenting cell </li></ul></ul><ul><ul><li>Cytotoxic (killer) T cells (CD8 cells) </li></ul></ul><ul><ul><li>Helper T cells (CD4 cells) </li></ul></ul><ul><ul><ul><li>The ones attacked in HIV infection </li></ul></ul></ul><ul><ul><li>Suppressor T cells </li></ul></ul><ul><ul><li>Memory T cells </li></ul></ul><ul><li>T cells are “blind” to free-floating antigens </li></ul>
    30. 31. What happens in a cell-mediated response? <ul><li>The key events: </li></ul><ul><ul><li>Surveillance and recognition </li></ul></ul><ul><ul><li>Attack </li></ul></ul><ul><ul><li>Memory </li></ul></ul>
    31. 32. What happens during surveillance? <ul><li>T cells (helper and cytotoxic) “feel” cells </li></ul><ul><ul><li>Check for MHC (hotdog bun) </li></ul></ul><ul><ul><ul><li>MHC = major histocompatibility complex </li></ul></ul></ul><ul><ul><ul><li>MHC-I on all cells </li></ul></ul></ul><ul><ul><ul><li>MHC-II only on APCs </li></ul></ul></ul><ul><ul><ul><li>HLA (human leukocyte antigen) group = MHC </li></ul></ul></ul>
    32. 33. What happens during surveillance? <ul><li>If T cell encounters APC (recognition): </li></ul><ul><ul><li>Notices a hotdog in the bun (antigen cradled in MHC) </li></ul></ul><ul><ul><li>Cytotoxic T cells only respond to MHC-I complex </li></ul></ul><ul><ul><li>Helper T cells only respond to MHC-II </li></ul></ul><ul><ul><li>APC then secretes interleukin-1 </li></ul></ul><ul><ul><ul><li>This stimulates T cells to divide </li></ul></ul></ul><ul><ul><ul><li>This launches immune response: ATTACK! </li></ul></ul></ul>
    33. 34. What happens during attack? <ul><li>Interleukins stimulate T cells, Helper T cells and (we’ll get to this later) B cells </li></ul><ul><li>The “right” T cells and helper T cells produce clones </li></ul><ul><ul><li>Cytotoxic clones use perforin to kill infected or cancerous cells (“ touch kill ”): </li></ul></ul><ul><ul><li>http://www.cellsalive.com/ctl.htm </li></ul></ul><ul><ul><li>http://www.cat.cc.md.us/courses/bio141/lecguide/unit3/cellular/cmidefense/ctls/ctlapop.html </li></ul></ul><ul><ul><li>Helper T cell clones stimulate more cytotoxic T cells (and B cells) </li></ul></ul>
    34. 35. What happens during the memory phase? <ul><li>During cloning, some T cells are put in reserve </li></ul><ul><ul><li>Thousands of these “hang out” in the body </li></ul></ul><ul><ul><li>Launch immediate attack if same antigen appears again </li></ul></ul><ul><ul><li>Attack is so quick, no symptoms develop </li></ul></ul>
    35. 36. Which of the following activates the cytotoxic T cells? <ul><li>A. Interferon </li></ul><ul><li>B. Interleukin-I </li></ul><ul><li>C. Interleukin-II </li></ul><ul><li>D. Interleukin-IV </li></ul>
    36. 37. T cells may produce _____ which is lethal to the target cells invaded by a pathogen <ul><li>A. Interleukin-II </li></ul><ul><li>B. Perforin </li></ul><ul><li>C. Interferon </li></ul><ul><li>D. Interleukin-IV </li></ul>
    37. 38. What happens in an antibody-mediated response? <ul><li>The key events: </li></ul><ul><ul><li>Recognition </li></ul></ul><ul><ul><li>Attack </li></ul></ul><ul><ul><li>Memory </li></ul></ul><ul><li>The key players: </li></ul><ul><ul><li>B cells (plasma and memory cells) </li></ul></ul><ul><ul><li>Helper T cells </li></ul></ul><ul><ul><li>Free-floating antigens </li></ul></ul>
    38. 39. What happens during recognition? <ul><li>Capping : free-floating antigen binds to B cell with correct antibody on its PM </li></ul><ul><li>Endocytosis of antigen-antibody complex </li></ul><ul><li>Display of hotdog + bun </li></ul><ul><ul><li>Helper T cell binds, secretes interleukin-2 </li></ul></ul><ul><ul><li>Gives B cell the “go” signal </li></ul></ul><ul><li>Clonal selection : only B cells with correct antibody clone </li></ul><ul><li>Plasma cell differentiation : large B cells with lots of rough ER </li></ul><ul><li>antigen presentation animation </li></ul>
    39. 40. What happens during attack? <ul><li>Plasma cells make millions of antibodies (IgM) and distribute in blood plasma </li></ul><ul><li>Antibodies incapacitate antigens: </li></ul><ul><ul><li>Agglutination </li></ul></ul><ul><ul><li>Neutralization </li></ul></ul><ul><ul><li>Precipitation </li></ul></ul><ul><ul><li>Complement fixation </li></ul></ul><ul><li>Eosinophils or T cells then destroy antigens </li></ul>
    40. 41. What happens during memory? <ul><li>Primary response (first exposure) </li></ul><ul><ul><li>takes 3 to 6 days to produce plasma cells </li></ul></ul><ul><li>Secondary response </li></ul><ul><ul><li>Memory B cells in reserve form plasma cells in mere hours </li></ul></ul><ul><ul><li>IgG produced to combat antigen </li></ul></ul>
    41. 42. If a patient has a high level of IgM in the blood, you can assume <ul><li>A. He has leukocytosis </li></ul><ul><li>B. He has just been infected with chicken pox for the first time </li></ul><ul><li>C. He has just been re-exposed to chicken pox </li></ul><ul><li>D. He is having a severe allergy attack </li></ul>
    42. 43. Only ______ can recognize MHC-II. <ul><li>A. B cells </li></ul><ul><li>B. Macrophages </li></ul><ul><li>C. Cytotoxic-T cells </li></ul><ul><li>D. Helper-T cells </li></ul>
    43. 44. Which is not a part of the recognition process? <ul><li>A. Display </li></ul><ul><li>B. Capping </li></ul><ul><li>C. Exocytosis </li></ul><ul><li>D. Clonal selection </li></ul>
    44. 45. Who can’t you do without in specific immunity? <ul><li>_________ cells are the lynch pins for both antibody- and cell-mediated immunity </li></ul><ul><li>Why? </li></ul>
    45. 46. Immunization and immune disorders
    46. 47. What is hypersensitivity? <ul><li>Excessive reaction to an antigen (allergen) to which most people do not react </li></ul><ul><ul><li>Includes </li></ul></ul><ul><ul><ul><li>Allergies </li></ul></ul></ul><ul><ul><ul><li>Alloimmunity (transplants) </li></ul></ul></ul><ul><ul><ul><li>Autoimmunity </li></ul></ul></ul><ul><ul><li>Four types </li></ul></ul>
    47. 48. What are the four types? <ul><li>Type I--Acute hypersensitivty </li></ul><ul><ul><li>IgE-mediated, often non-dosage dependent </li></ul></ul><ul><ul><li>Degranualation of basophils and mast cells </li></ul></ul><ul><ul><li>Food allergies, asthma, anaphylaxis (severe type I) </li></ul></ul><ul><li>Type II--antibody-dependent cytotoxic hypersensitivity </li></ul><ul><ul><li>IgG ir IgM attacks antigens bound on a cell surface </li></ul></ul><ul><ul><ul><li>Blood transfusion reactions, penicillin allergy, some drugs, toxic goiter, myasthenia gravis </li></ul></ul></ul>
    48. 49. What are the four types? <ul><li>Type III: immune complex hypersensitivity </li></ul><ul><ul><li>IgG or IgM bind directly to free-floating antigens causing precipitation in blood or tissues </li></ul></ul><ul><ul><ul><li>This activates complement and inflammation </li></ul></ul></ul><ul><ul><ul><li>Necrosis follows </li></ul></ul></ul><ul><ul><li>Some autoimmmune diseases (e.g. lupus, glomerularnephritis) </li></ul></ul><ul><li>Type IV: delayed hypersensitivity </li></ul><ul><ul><li>Cell-mediated, after 1/2 to 3 days </li></ul></ul><ul><ul><li>APCS display antigen to CD4 cells, which activate CD8 cells: specific and non-specific responses </li></ul></ul><ul><ul><li>Allergies to haptens (poison oak, make-up), graft rejection, TB skin test, type I diabetes </li></ul></ul>
    49. 50. What is immunization? <ul><li>Active immunization </li></ul><ul><ul><li>Vaccine prompts antibody manufacture </li></ul></ul><ul><ul><ul><li>Also creates B memory cells </li></ul></ul></ul><ul><ul><ul><li>Lasts for years </li></ul></ul></ul><ul><li>Passive immunization </li></ul><ul><ul><li>Injection of antibodies (gamma globulin serum) </li></ul></ul><ul><ul><ul><li>Also breastfeeding </li></ul></ul></ul><ul><ul><li>Can prevent infection after exposure </li></ul></ul><ul><ul><li>Antibodies eventually degrade </li></ul></ul><ul><ul><li>No memory B cells formed </li></ul></ul>vaccination movie
    50. 51. Naturally acquired passive immunity results from <ul><li>A. A bee sting </li></ul><ul><li>B. Immunization </li></ul><ul><li>C. A flu shot </li></ul><ul><li>D. Placental transfer </li></ul>
    51. 52. During type II hypersensitivity <ul><li>A. Immuniglobins attack antigens bound to a cell </li></ul><ul><li>B. A cell-mediated response happens days after exposure </li></ul><ul><li>C. Anaphylaxis is common </li></ul><ul><li>D. Immuniglobins bind to free-floating antigens causing inflammation </li></ul>
    52. 53. Why are organ transplants often rejected? <ul><li>T-cells attack foreign cell, kill them </li></ul><ul><ul><li>Immunosuppresive drugs counteract this </li></ul></ul><ul><ul><li>Problem: may have to take these drugs for rest of life </li></ul></ul><ul><li>Future therapy: add FasL markers to transplanted cells </li></ul><ul><ul><li>When T-cells w/Fas markers contact FasL, they commit cell suicide (apoptosis) </li></ul></ul><ul><ul><li>http://www.cat.cc.md.us/courses/bio141/lecguide/unit3/cellular/cmidefense/ctls/fasan.html </li></ul></ul><ul><ul><li>This is what naturally occurs in the testes, anterior chamber of eye, brain (immunologically privileged areas) </li></ul></ul>
    53. 54. What are autoimmune diseases? <ul><li>Self-attack by immune system </li></ul><ul><ul><li>Produce autoantibodies </li></ul></ul><ul><li>Lupus erythematosus: inflammation of CTs </li></ul><ul><ul><li>Fever, fatigue, joint pain, light sensitivity </li></ul></ul><ul><li>Rheumatic fever: antibodies attack mitral and aortic valves </li></ul><ul><li>Others: rheumatoid arthritis, Type I diabetes, multiple sclerosis, Grave’s disease </li></ul>
    54. 55. What are immunodeficiency diseases? <ul><li>Immune system weakened or fails to respond </li></ul><ul><li>Severe combines immunodeficiency disease (SCID) </li></ul><ul><ul><li>Rare/absent T and B cells (hereditary) </li></ul></ul><ul><li>Acquired immunodeficiency syndrome (AIDS) </li></ul><ul><ul><li>Develops from HIV infection </li></ul></ul>
    55. 56. How does HIV cause AIDS? <ul><li>HIV: a retrovirus </li></ul><ul><ul><li>What does this mean? </li></ul></ul><ul><ul><li>Extremely high mutation rate </li></ul></ul><ul><li>Infects helper T cells, neutrophils, macrophages </li></ul><ul><ul><li>Recall: helper Ts needed to stimulate both T and B cells </li></ul></ul><ul><ul><ul><li>Infects only a small number of helper Ts though </li></ul></ul></ul><ul><ul><ul><ul><li>Possibly infected cells have FasL which destroys healthy helper Ts </li></ul></ul></ul></ul><ul><li>Incubation: several months to years </li></ul><ul><ul><li>Final stages: AIDS </li></ul></ul><ul><ul><ul><li>No immune response capability </li></ul></ul></ul><ul><ul><ul><li>Kaposi’s sarcoma common </li></ul></ul></ul>
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