Mechanisms of Antibody-Mediated Tissue Injury and Disease
المؤلف:
Abbas, A. K., Lichtman, A. H., & Pillai, S
المصدر:
Basic Immunology : Function and disorders of immune system
الجزء والصفحة:
6th ed , page 226-227
2025-06-09
671
Antibodies specific for cell and tissue antigens may deposit in tissues and cause injury by inducing local inflammation, they may induce phagocytosis and destruction of cells, or they interfere with normal cellular functions (Fig. 1).
Fig1. Effector mechanisms of antibody-mediated diseases. Antibodies cause disease by A, Inducing inflammation at the site of deposition; B, Opsonizing cells (such as red cells) for phagocytosis; and C, Interfering with normal cellular functions, such as hormone receptor signaling. All three mechanisms are seen with antibodies that bind directly to their target antigens, but immune complexes cause disease mainly by inducing inflammation (A). TSH, Thyroid-stimulating hormone.
• Inflammation. Antibodies against tissue antigens induce inflammation by attracting and activating leukocytes. IgG antibodies of the IgG1 and IgG3 subclasses bind to neutrophil and macrophage Fc receptors and activate these leukocytes, resulting in inflammation . The same antibodies, as well as IgM, activate the complement system by the classical pathway, resulting in the production of complement by-products that recruit leukocytes and induce inflammation. When leukocytes are activated at sites of antibody deposition, these cells release reactive oxygen species and lysosomal enzymes that damage the adjacent tissues.
• Opsonization and phagocytosis. If antibodies bind to cells, such as erythrocytes, neutrophils, and plate lets, the cells are opsonized and may be ingested and destroyed by host phagocytes.
• Abnormal cellular responses. Some antibodies may cause disease without directly inducing tissue injury. For example, in pernicious anemia, autoantibodies specific for a protein required for absorption of vitamin B12 cause a multisystem disease due to B12 deficiency. In some cases of myasthenia gravis, antibodies against the acetylcholine receptor inhibit neuromuscular transmission, causing paralysis. Other antibodies may directly activate receptors, mimicking their physiologic ligands. The only known example is a form of hyperthyroidism called Graves disease, in which antibodies against the receptor for thyroid-stimulating hormone activate thyroid cells even in the absence of the hormone.
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