Examples and Treatment of Diseases Caused by Cell- or Tissue-Specific Antibodies
المؤلف:
Abbas, A. K., Lichtman, A. H., & Pillai, S
المصدر:
Basic Immunology : Function and disorders of immune system
الجزء والصفحة:
6th ed , page 228-229
2025-06-09
731
Antibodies specific for cell and tissue antigens are the cause of many human diseases, involving blood cells, heart, kidney, lung, and skin (Fig. 1). Examples of anti-tissue antibodies are those that react with the glomerular basement membrane and induce inflammation, a form of glomerulonephritis. Antibodies against cells include those that opsonize blood cells and target them for phagocytosis, as in autoimmune hemolytic anemia (red cell destruction) and autoimmune thrombocytopenia (destruction of platelets). Antibodies that interfere with hormones or their receptors were mentioned earlier. In most of these cases, the antibodies are autoantibodies, but less commonly, antibodies produced against a microbe may cross-react with an antigen in the tissues. For instance, in rare instances, streptococcal infection stimulates the pro duction of antibacterial antibodies that cross-react with antigens in the heart, producing the cardiac inflammation that is characteristic of rheumatic fever.
Fig1. Human antibody-mediated diseases (type II hypersensitivity). The figure lists examples of human diseases caused by antibodies. In most of these diseases, the role of antibodies is inferred from the detection of antibodies in the blood or the lesions, and in some cases by similarities with experimental models in which the involvement of antibodies can be formally established by transfer studies.
Therapy for antibody-mediated diseases is intended mainly to limit inflammation and its injurious consequences with drugs such as corticosteroids. In severe cases, plasmapheresis is used to reduce levels of circulating antibodies. In hemolytic anemia and thrombocytopenia, splenectomy is of clinical benefit because the spleen is the major organ where opsonized blood cells are phagocytosed. Some of these diseases respond well to treatment with intravenous IgG (IVIG) pooled from healthy donors. How IVIG works is not known; it may bind to the inhibitory Fc receptor on myeloid cells and B cells and thus block activation of these cells (see Chapter 7, Fig. 7.15), or it may reduce the half-life of pathogenic antibodies by competing for binding to the neonatal Fc receptor in endothelial cells and macrophages . Treatment of patients with an antibody specific for CD20, a surface protein of mature B cells, results in depletion of the B cells and may be useful for treating some antibody-mediated disorders. Other approaches in development for inhibiting the production of autoantibodies include treating patients with antibodies that block CD40 or its ligand and thus inhibit helper T cell–dependent B cell activation and antibodies to block cytokines that promote the survival of B cells and plasma cells. There is also interest in inducing tolerance in cases in which the autoantigens are known.
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