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Francisco G. La Rosa, MD III. Immune mechanisms of tissue injury A. Type I: Anaphylaxis or Immediate Hypersensitivity Reactions B. Type II: Cytolytic Antibody Reactions C. Type III: Immune Complex Mediated Reactions D. Type IV: Cell Mediated Reactions
Although the immune system generally is protective, the same immunologic mechanisms that defend the host at times may result in severe damage to tissues and, occasionally, may cause death. Cell and Coombs have classified these damaging immunologic reactions (also called hypersensitivity reactions) into four major types: immediate hypersensitivity (type I) reactions, cytotoxic (type II) reactions, immune complex-mediated (type III) reactions, and delayed hypersensitivity (cellmediated, type IV) reactions.
by mucous glands.
Genetic factors: Hay fever, asthma, and food allergies, show familial
tendency.
Therapy: 1. Avoidance 2. Hyposensitization 3. Administration of modified allergens, or "allergoids". 4. Drug treatment a. Diphenhydramine b. Corticosteroids c. Epinephrine
Type II hypersensitivity reactions: 1. Transfusion reactions: Intravascular hemolysis of red blood cells
usually is associated with ABO system incompatibility.
5. White blood cell lysis a. Systemic lupus erythematosus (SLE) b. Granulocytopenia c. Idiopathic thrombocytopenic purpura (ITP) 6. Nephrotoxic nephritis. Goodpasture's syndrome 7. Bullous diseases. Characterized by antibody and complement
deposition in squamous intercellular spaces and along the basement
Therapy for cytotoxic reactions: 1. Suppression of the immune response. 2. Removal of offending antibodies. 3. Withholding the offending antibodies. 4. Nephrectomy. C. Type III: Immune Complex Mediated Reactions
The pathogenesis of immune complex disorders involves an interplay of antigen, antibody, complement, and neutrophils. Soluble immune complexes: Generally occurs in the region of antigen excess. Virtually any antigen that induces a detectable antibody response will serve. The antibodies involved are primarily precipitating IgG and IgM capable of fixing complement. Immune adherence: Being soluble, the immune complexes escape phagocytosis, penetrate the endothelium of blood vessel walls (probably with the aid of vasoactive amines released from platelets and basophils), and are deposited on the vascular basement membrane. Complement activation: In the formation of immune complexes, complement is activated with the release of factors that are chemotactic for neutrophils (i.e., C5a and C5b67); the neutrophils then infiltrate the area and release lysosomal enzymes that destroy the basement membrane of the vessels.
1. Arthus reaction 2. Serum sickness 3. Hypersensitivity pneumonitis 4. Poststreptococcal glomerulonephritis 5. Autoimmune disease. Rheumatoid arthritis and SLE. D. Type IV: Cell Mediated Reactions
Delayed hypersensitivity (cell-mediated) tissue damage results from the interaction between sensitized T cells and specific antigen, which leads to the release of soluble effector substances called lymphokines, direct cytotoxicity, or both. This reaction is independent of antibody and complement but is dependent upon two types of functioning T cells: T4 + cells. Cells for delayed hypersensitivity and cells that help to produce
cytotoxic/suppressor and T8 + cells. Mediators of delayed hypersensitivity: It is known how many biochemically distinct lymphokines exist; however, the following are among those functionally recognized:
1. Migration inhibition factor (MIF) inhibits migration of macrophages. 2. Macrophage activation factor (MAF) enhances microbicidal and
cytolytic activity of macrophages (IFN).
3. Macrophage chemotactic factor stimulates infiltration of macrophages. 4. Transfer factor 5. Leukocyte inhibition factor (LIF) inhibits random migration of
neutrophils.
7. Lymphotoxin has the ability to lyse certain tumor cells. 8. Gamma interferon functions similarly to MAF. a. Rejection of grafted tissues and organs. b. Contact dermatitis c. Autoimmune disease Modulation of delayed hypersensitivity. 1. Suppressant agents a. Corticosteroids b. Antilymphocyte, or antithymocyte, serum