Human Anatomy & Physiology (9th Edition)

Published by Pearson
ISBN 10: 0321743261
ISBN 13: 978-0-32174-326-8

Chapter 21 - The Immune System: Innate and Adaptive Body Defenses - Review Questions - Page 799: 29


Hypersensitivity is a condition of heightened alertness in which the immune system damages normal tissues as it fights off a perceived injurious substance which is intrinsically harmless to the body. Hypersensitivities may be divided into three classes: type one is immediate hypersensitivities; type II is subacute hypersensitivities -- including cytotoxic and immune complex hypersensitivities, and type III which covers delayed hypersensitivities. In immediate hypersensitivity reactions, antibodies (IgE) are the main effectors. This is also the case in subacute hypersensitivities (IgG and IgM). In contrast, T-cells are the major actors in delayed hypersensitivities. Most of these reactions can be classified as allergic responses. Some common signs and symptoms of allergic reactions are respiratory difficulties-- as in asthma--, and gastrointestinal problems such as cramping, diarrhea and vomiting. Allergies are not usually life-threatening but anaphylactic reactions can be fatal, if not treated promptly. In anaphylaxis, the toxin or antigen is introduced directly into the blood stream by a bee sting , a spider bite, or by a hypodermic needle (penicillin injection). As the toxin spreads quickly all over the body, it induces a severe, intense, immunological reaction that is potentially fatal ,

Work Step by Step

There are two sub-types of sub-acute hypersensitivities; the cytotoxic and the immune complex mediated. In cytotoxic hypersensitivities the effector mechanism involves antibody-induced phagocytosis and complement-mediated lysis of cellular antigens. This type of hypersensitivity functions in conditions like erythroblastosis fetalis, and in mismatched blood transfusions. IgG and IgM antibodies are involved in these reactions. In the other subclass of subacute hypersensitivities, widely-distributed antigens form bodywide immune complexes with antibodies. The response of the body is an intense complement-mediated killing of neutrophils and widespread tissue damage. Examples of this kind of hypersensitivity are farmer's lung and glomerulonephritis in systemic glomerulonephritis (SLE). Delayed hypersensitivity is primarily cell mediated, and is of slow onset (1-3) days. The chief effectors are cytokine activated macrophages, and cytotoxic T-cells. Examples of this kind of hypersensitivity are dermatitidess triggered by contacts with substances such as poison ivy, nickel, chemicals in cosmetics or deodorants. The tuberculin reaction to dead or partially killed tuberculosis bacteria is also a delayed hypersensitivity reaction.
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