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Immunologic Disorders

Immunologic Disorders. Chapter 18. Type I Hypersensitivities: Immediate IgE-Mediated. IgE causes immediate (type I) hypersensitivities Characterized by immediate reaction of the sensitized individual Generally within minutes of exposure

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Immunologic Disorders

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  1. Immunologic Disorders Chapter 18

  2. Type I Hypersensitivities:Immediate IgE-Mediated • IgE causes immediate (type I) hypersensitivities • Characterized by immediate reaction of the sensitized individual • Generally within minutes of exposure • Tendency to have type I hypersensitivities is inherited • Reactions occur in at least 20% to 30% of population

  3. Type I Hypersensitivities:Immediate IgE-Mediated • Sensitization occurs when antigen makes contact with some part of body and induces response • IgE antibodies bind to receptors on mast cells and basophiles • Antigen readily bonds to cells fixed with IgE antibodies • Within seconds, mast cells degranulate releasing mediators that initiate immune reaction including hives, hay fever and anaphylaxis

  4. Type I Hypersensitivities:Immediate IgE-Mediated • Localized anaphylaxis • Most allergic reactions are local anaphylaxis • Hives • Allergic skin condition characterized by formation of wheal and flare rash • Hay fever • Allergic condition caused by inhaled antigen • Condition marked by itching teary eyes, sneezing and runny nose • Asthma • Respiratory allergy • Allergic mediators attracted to inflamed respiratory tract • Results in increased mucous secretion and bronchi spasm

  5. Type I Hypersensitivities:Immediate IgE-Mediated • Generalized anaphylaxis • Rare, but more serious • Antigen enters bloodstream and becomes widespread • Reactions affect almost entire body • Can induce shock • Massive release of mediators causes extensive blood vessel dilation and fluid loss • Causes fall in pressure leading to blood flow insufficiency

  6. Type I Hypersensitivities:Immediate IgE-Mediated • Immunotherapy • General term for techniques used to modify immune system for favorable effect • Procedure is to inject individual with extremely dilute suspension of allergen • Called desensitization or hyposensitization • Concentration of allergen gradually increased over time • Individual gradually becomes less sensitive

  7. Type I Hypersensitivities:Immediate IgE-Mediated • Immunotherapy • Second therapeutic procedure is injection of antibodies to bind IgE • Essentially anti-IgE antibodies • Most IgE are bound to mast cells and basophiles • Engineered anti-IgE created • rhuMab = recombinant human Monoclonal antibody

  8. Type II Hypersensitivities: Cytotoxic • Complement-fixing antibodies react with cell surface antigens causing cell injury or death • Cells can be destroyed in type II reactions through complement fixation and antibody-dependent cellular cytotoxicity (ADCC) • Examples of type II hypersensitivities are • Transfusion reactions • Hemolytic disease of the newborn

  9. Type II Hypersensitivities: Cytotoxic • Transfusion reactions • Normal red blood cells have different surface antigens • Antigens differ from person to person • People are designated type A, B, AB or O • Transfused blood that is antigenically different can be lysed by recipient immune cells • Cross-matching blood is used to ensure compatibility between donor and recipient • Antibody-coated cells removed by phagocyte system • Symptoms include low blood pressure, pain, nausea and vomiting

  10. Type II Hypersensitivities: Cytotoxic • Hemolytic disease of the newborn • Basis of disease is incompatibility of Rh factor between mother and child • Rh factor RBC cell surface antigen • Rh positive = Rh antigen present • Rh negative = Rh antigen missing • Anti-Rh antibodies form in Rh negative mother pregnant with Rh positive fetus • First Rh positive fetus unharmed • Second Rh positive fetus provokes strong secondary immune response • IgG antibodies of secondary response cross placenta causing extensive damage to fetal red blood cells

  11. Type III Hypersensitivities:Immune Complex-Mediated • Immune complexes consist of antigen and antibody bound together • Usually adhere to Fc receptors on cells • Complexes are destroyed and removed • Certain instances complexes persist in circulation or at sites of formation • Initiate blood clotting mechanism • Activate complement contributing to inflammation • Complexes commonly deposited in skin, joints and kidney • Complexes also cause disseminated intravascular coagulation (DIC) • Clots in small vessels • Leads to system failure

  12. Type IV Hypersensitivities:Delayed Cell-Mediated • Delayed hypersensitivities caused by cell-mediated immunity • Slowly developing response to antigen • Reactions peak in 2 to 3 days instead of minutes • T cells are responsible for reactions • Reactions can occur nearly anywhere in the body • Delayed hypersensitivity reactions responsible for contact dermatitis, tissue damage, rejection of tissue grafts and some autoimmune diseases

  13. Type IV Hypersensitivities:Delayed Cell-Mediated • Tuberculin skin test • Test involves introduction of small quantities of protein antigens from tubercle bacillus into skin • In positive skin test injection site reddens and gradually thickens • Reaction reaches peak in 2 to 3 days • Reactions result from sensitized T cells, release of cytokines and influx of macrophages

  14. Type IV Hypersensitivities:Delayed Cell-Mediated • Contact hypersensitivities • Mediated by the T cells • T cells release cytokines • Cytokines initiate inflammation that attracts macrophages • Macrophages release mediators to add to inflammation • Common examples of contact allergies include • Poison ivy and poison oak • Nickel in metal jewelry • Chromium salts in leather • Latex products

  15. Transplant Immunity • Major drawback to graft transplantation is possible immunological rejection • Differences between donor and recipient tissues basis for rejection • Rejection is predominantly type IV reaction • Killing of graft cells occurs through complex combination of mechanisms • Contact with sensitized cytotoxic T cells and natural killer cells • Combination of agents commonly used to prevent graft rejection • Cyclosporin A • Steroids • Basiliximab • Monoclonal antibody preparation • Blocks binding of immune mediators

  16. Autoimmune Diseases • Body usually recognizes self antigens • Destroys lymphocytes that would destroy self • Malfunction in immune recognition basis for autoimmunity • Autoimmune diseases may result from reactions to antigens that are similar to self antigens • Autoimmunity may occur after tissue injury • Self antigens released from injured organ • Autoantibodies form and interact with injured tissues and cause further damage

  17. Autoimmune Diseases • Spectrum of autoimmune diseases • Reactions occur over spectrum • Organ-specific to widespread responses • Organ-specific • Thyroid disease • Only thyroid is affected • Widespread response • Lupus • Autoantibodies made against nuclear constituents of all body cells • Rheumatoid arthritis • Immune response made against collagen in connective tissue • Myasthenia gravis • Autoantibody-mediated disease • Antibody to acetylcholine receptor proteins

  18. Autoimmune Diseases • Treatment of autoimmune diseases • Treatment aimed at: • Killing dividing cells • Immunosuppressant • Controlling T cell signaling • Cyclosporin • Anti-inflammatory medications • Cortisone-like steroids • Replacement therapy • Insulin

  19. Immunodeficiency Disorders • Immunodeficiency disorders are marked by the body’s inability to make and sustain an adequate immune response • Two basic types of disorders • Primary or congenital • Inborn as a result of genetic defect or developmental abnormality • Secondary or acquired • Can be acquired as result of infection or other stressor

  20. Immunodeficiency Disorders • Primary immunodeficiencies • Generally rare • Examples • Agammaglobulinemia • Few or no antibodies produced • Occurs in 1 in 50,000 people • Severe combined immunodeficiency disorder (SCID) • Neither B nor T lymphocytes are functional • Occurs in 1 in 500,000 live births • Selective IgA deficiency • Little or no IgA produced • Most common disorder • One in 333 to 700 people

  21. Immunodeficiency Disorders • Secondary immunodeficiencies • Result from environmental, rather than genetic factors • Malignancies, advanced age certain infections, immunosuppressive drugs and malnutrition are just a few • Often results from depletion of certain cells of the immune system • Syphilis, leprosy and malaria affect T-cell population and macrophage function • Malignancies of lymphoid system decrease antibody-mediated immunity • Most serious widespread immunodeficiency is AIDS • Destroys helper T cells • Inhibits initiation of cellular and antibody-mediated immunity

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