Microbiology Chapter 19 Outline
Introduction (p. 515) 1. Hay fever, transplant rejection, and autoimmunity are examples of harmful immune reactions. 2. Immunosuppression is inhibition of the immune system. 3. Superantigens activate many T cell receptors that can cause adverse host responses.
Hypersensitivity (pp. 516–526) 1. Hypersensitivity reactions represent immunological responses to an antigen (allergen) that lead to tissue damage rather than immunity. 2. Hypersensitivity reactions occur when a person has been sensitized to an antigen. 3. Hypersensitivity reactions can be divided into four classes: types I, II, and III are immediate reactions based on humoral immunity, and type IV is a delayed reaction based on cell-mediated immunity.
Allergies and the Microbiome (p. 516) 4. Childhood exposure to microbes may decrease development of allergies.
Type I (Anaphylactic) Reactions (pp. 516–522) 5. Anaphylactic reactions involve the production of IgE antibodies that bind to mast cells and basophils to sensitize the host. 6. The binding of two adjacent IgE antibodies to an antigen causes the target cell to release chemical mediators, such as histamine, leukotrienes, and prostaglandins, which cause the observed allergic reactions. 7. Systemic anaphylaxis may develop in minutes after injection or ingestion of the antigen; this may result in circulatory collapse and death. 8. Localized anaphylaxis is exemplified by hives, hay fever, and asthma. 9. Skin testing is useful in determining sensitivity to an antigen. 10. Desensitization to an antigen can be achieved by repeated injections of the antigen, which leads to the formation of blocking (IgG) antibodies.
Microbiology Chapter 19 Outline
Type II (Cytotoxic) Reactions (pp. 522–524) 11. Type II reactions are mediated by IgG or IgM antibodies and complement. 12. The antibodies are directed toward foreign cells or host cells. Complement fixation may result in cell lysis. Macrophages and other cells may also damage the antibody-coated cells. 13. Human blood may be grouped into four principal types, designated A, B, AB, and O. 14. The presence or absence of two carbohydrate antigens designated A and B on the surface of the red blood cell determines a person’s blood type. 15. Naturally occurring antibodies are present in serum against the opposite AB antigen. 16. Incompatible blood transfusions lead to the complement-mediated lysis of the donor red blood cells. 17. The absence of the Rh antigen in certain individuals (Rh− ) can lead to sensitization upon exposure to it. 18. An Rh+ person can receive Rh+ or Rh− blood transfusions. 19. When an Rh− person receives Rh+ blood, that person will produce anti-Rh antibodies. Subsequent exposure to Rh+ cells will result in a rapid, serious hemolytic reaction. 20. An Rh− mother carrying an Rh+ fetus will produce anti-Rh antibodies. Subsequent pregnancies involving Rh incompatibility may result in hemolytic disease of the newborn. 21. HDNB may be prevented by passive immunization of the mother with anti-Rh antibodies. 22. In the disease thrombocytopenic purpura, platelets are destroyed by antibodies and complement. 23. Agranulocytosis and hemolytic anemia result from antibodies against one’s own blood cells coated with drug molecules.
Type III (Immune Complex) Reactions (pp. 524–525) 24. Immune complex diseases occur when IgG antibodies and soluble antigen form small complexes that lodge in the basement membranes of cells. 25. Subsequent complement fixation results in inflammation. 26. Glomerulonephritis is an immune complex disease.
Type IV (Delayed Cell-Mediated) Reactions (pp. 525–526) 27. Delayed cell-mediated hypersensitivity reactions are due primarily to T cell proliferation. 28. Sensitized T cells secrete cytokines in response to the appropriate antigen. 29. Cytokines attract and activate macrophages and initiate tissue damage. 30. The tuberculin skin test and allergic contact dermatitis are examples of delayed hypersensitivities. Microbiology Chapter 19 Outline
Autoimmune Diseases (pp. 526–528) 1. Autoimmunity results from a loss of self-tolerance. 2. Self-tolerance occurs during fetal development; T cells that will target host cells are eliminated (clonal deletion) or inactivated. 3. Autoimmunity may be due to antibodies against infectious agents. 4. Graves’ disease and myasthenia gravis are cytotoxic autoimmune reactions in which antibodies react to cell-surface antigens. 5. Systemic lupus erythematosus and rheumatoid arthritis are immune complex autoimmune reactions in which the deposition of immune complexes results in tissue damage. 6. Multiple sclerosis, insulin-dependent diabetes mellitus, and psoriasis are cell-mediated autoimmune reactions mediated by T cells.
Reactions Related to the Human Leukocyte Antigen (HLA) Complex (pp. 528–532) 1. MHC self molecules located on cell surfaces express genetic differences among individuals; these antigens are called HLAs in humans. 2. To prevent the rejection of transplants, HLA and ABO blood group antigens of the donor and recipient are matched as closely as possible. 3. Transplants recognized as foreign antigens may be lysed by T cells and attacked by macrophages and complement-fixing antibodies. 4. Transplantation to a privileged site (such as the cornea) or of a privileged tissue (such as pig heart valves) does not cause an immune response. 5. Pluripotent stem cells differentiate into a variety of tissues that may provide tissues for transplant. 6. Four types of transplants have been defined on the basis of genetic relationships between the donor and the recipient: autografts, isografts, allografts, and xenotransplants. 7. Bone marrow transplants (with immunocompetent cells) can cause graft-versus-host disease. 8. Successful transplant surgery often requires immunosuppressant drugs to prevent an immune response to the transplanted tissue.
Microbiology Chapter 19 Outline
The Immune System and Cancer (pp. 532–533) 1. Cancer cells are normal cells that have undergone transformation, divide uncontrollably, and possess tumor-associated antigens. 2. The response of the immune system to cancer is called immunological surveillance.
3. TC cells recognize and lyse cancerous cells. 4. Cancer cells can escape detection and destruction by the immune system. 5. Cancer cells may grow faster than the immune system can respond.
Immunotherapy for Cancer (pp. 532–533) 6. Vaccines against liver and cervical cancer are available; a therapeutic vaccine against prostate cancer also has been approved. 7. Herceptin consists of monoclonal antibodies against a breast cancer growth factor. 8. Immunotoxins are chemical poisons linked to a monoclonal antibody; the antibody selectively locates the cancer cell for release of the poison.
Immunodeficiencies (pp. 533–534) 1. Immunodeficiencies can be congenital or acquired. 2. Congenital immunodeficiencies are due to defective or absent genes. 3. A variety of drugs, cancers, and infectious diseases can cause acquired immunodeficiencies.
Acquired Immunodeficiency Syndrome (AIDS) (pp. 534–544) The Origin of AIDS (p. 535) 1. HIV is thought to have originated in central Africa and was brought to other countries by modern transportation and unsafe sexual practices.
HIV Infection (pp. 535–540) 2. AIDS is the final stage of HIV infection. 3. HIV is a retrovirus with single-stranded RNA, reverse transcriptase, and a phospholipid envelope with gp120 spikes. 4. HIV spikes attach to CD4+ and coreceptors on host cells; the CD4+ receptor is found on T helper cells, macrophages, and dendritic cells. 5. Viral RNA is transcribed to DNA by reverse transcriptase. The viral DNA becomes integrated into the host chromosome to direct synthesis of new viruses or to remain latent as a provirus. Microbiology Chapter 19 Outline
6. HIV evades the immune system in latency, in vacuoles, by using cell–cell fusion, and by antigenic change. 7. HIV-1 accounts for most HIV infections. Subtype B of HIV-1 is the most common type in the United States. 8. HIV infection is categorized by symptoms: phase 1 (asymptomatic), phase 2 (indicator opportunistic infections), and phase 3 (CD4+ cells <200 cells/μ1). 9. The progression from HIV infection to AIDS takes about 10 years. 10. The life of an AIDS patient can be prolonged by the proper treatment of opportunistic infections. 11. People lacking CCR5 are resistant to HIV infection. 12. Elite controllers are long-term survivors who may hold the key to HIV treatment.
Diagnostic Methods (pp. 540–541) 13. HIV antibodies are detected by ELISA and Western blotting. 14. Plasma viral load tests detect viral nucleic acid and are used to quantify HIV in blood.
HIV Transmission (p. 541) 15. HIV is transmitted by sexual contact, breast milk, contaminated needles, transplacental infection, artificial insemination, and blood transfusion. 16. In developed countries, blood transfusions are not a likely source of infection because blood is tested for HIV antibodies.
AIDS Worldwide (p. 541) 17. Heterosexual intercourse is the primary method of HIV transmission.
Preventing and Treating AIDS (pp. 542–544) 18. Discouraging sexual promiscuity and using condoms and sterile needles prevent the transmission of HIV. 19. Vaccine development is difficult because the virus remains inside host cells and there is no model of natural immunity to mimic. 20. Current chemotherapeutic agents target the virus enzymes, including reverse transcriptase, integrase, and protease. Other inhibitors include cell entry inhibitors, maturation inhibitors, and tetherins.