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BIOL 3120 (12)
Chapter 12

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Department
Biology
Course
BIOL 3120
Professor
Tanya Da Sylva
Semester
Fall

Description
Learning Objectives Chapter 12 •Define allergens and allergy. Explain what it means to be “sensitized” to an antigen.  certain kinds of innocuous molecule stimulatean adaptive immune response and the development of immunological memory in predisposed members of the population. On subsequent exposures to the antigen the immune memory produces inflammation and tissue damage that is at best an irritation, and at worst a threat to life. The person feels ill, as though fighting off an infection, when no infection exists. The overreactions of the immune system to harmless environmental antigens are called either hypersensitivity reactions or allergic reactions. The environmental antigens that cause these reactions are termed allergens and they induce a state of hypersensitivity or allergy •Distinguish between Types I, II, III and IV hypersensitivities with respect to immune reactant, antigen and effector mechanism; give one example of each (examples can be found in Fig 12.2).  encountered. Type I hypersensitivity reactions result from the binding of antigen to antigen- specific IgE bound to its Fc receptor, principally on mast cells. This interaction causes the degranulation of mast cells and the release of inflammatory mediators . Type I reactions are commonly caused by inhaled particulate antigens, of which plant pollens are good examples. Type I reactions have effects of varying severity, ranging from a runny nose to breathing difficulties and even death by asphyxiation. Type I hypersensitivity reactions are also described as immediate hypersensitivity because they occur immediately on exposure to antigen.  Type II hypersensitivity reactions are caused by small molecules that bond covalently to cell-surface components of human cells, producing modified structures that are perceived as foreign by the immune system. The B-cell response to these new epitopes produces IgG, which on binding to the modified cells causes their destruction through complement activation and phagocytosis. The antibiotic penicillin is an example of a small reactive molecule that can induce a type II hypersensitivity reaction.  Type III hypersensitivity reactions are due to small soluble immune complexes formed by soluble protein antigens binding to the IgG made against them. Some of these immune complexes become deposited in the walls of small blood vessels or the alveoli of the lungs. The immune complexes activate complement and initiate an inflammatory response that damages the tissue, impairing its physiological function. When antibodies or other proteins derived from nonhuman animal species are given therapeutically to patients, type III hypersensitivity reactions are a potential side-effect.  The effector molecules initiating type 1, II, and III hypersensitivity reactions are all antibodies. In contrast, type IV hypersensitivity reactions are caused by the products of antigen-specific effector T cells. Most reactions are caused by CD4 THl cells. For example, the inflammatory reaction around the site of an insect bite or sting is caused by CD4 THl cells that respond to peptide epitopes derived from venom and other insect proteins introduced by the bite. A minority of type IV hypersensitivity reactions are due to cytotoxic CD8 T cells. They arise when small, reactive, lipid-soluble molecules pass through cell membranes and bond covalently to intracellular human proteins.Degradation of these chemically modified proteins yields abnormal peptides that bind to HLA class 1 molecules and stimulate a cytotoxic T-cell response. For example, the allergic response to poison ivy involves cytotoxic T cells. These recognize peptides derived from intracellular proteins that are modified by chemical reaction with pentadecacatechol, a chemical acquired by touching the plant's leaves. Type IV hypersensitivity reactions are also described as delayed-type hypersensitivity or DTH because they are only manifested 1-3 days after exposure to antigen . •Describe a typical Type I hypersensitivity response. Start with sensitization to antigen and use the terms IgE, FceRI, mast cells, inflammatory mediators, eosinophils and basophils. Explain how basophils can aid in driving further TH2 (IgE) responses. •Describe the course of a typical IgE mediated allergic response (Type I hypersensitivity). Explain why an IgE mediated response can lead to such varied physical effects. •Describe the three strategies used to reduce the effects of allergic disease (Type I).  A prerequisite for a type 1 hypersensitivity reaction is that IgE antibody is made when a person first encounters the antigen. This is how the person becomes sensitized to the antigen. IgE differs from other antibody isotypes in being located predominantly in tissues, where it is bound to mast cells by high-affinity surface receptors known as FCERI.  IgE antibody causes allergic reactions because of its exceptionally high affinity for its Fc receptor  Also, unlike most other isotypes, IgE binds to its receptor in the absence of antigen. FCERI is expressed constitutively by mast cells and basophils, and by eosinophils. after they have been activated by cytokines.  All these cells have granules containing preformed inflammatory mediators. •Explain how drug treatments can trigger Type II hypersensitivity reactions.  Occasional side-effects seen after the administration of certain drugs are hemolytic anemia caused by the destruction of red blood cells, and thrombocytopenia caused by the destruction of platelets. These are examples of type II hypersensitivity reactions and have been associated with the antibiotic penicillin, quinidine (a drug used to treat cardiac arrhythmia), and methyldopa, which is used to reduce high blood pressure. In each case,
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