Th1 cells appear to be critical in effecting an antigen-specific phagocytic-mediated defence against microorganisms, principally bacteria, fungi and some parasites. If, however, Thl-biased immunity is directed against self-antigens, extensive tissue destruction and autoimmune disease may ensue. Common autoimmune diseases resulting from inappropriate Th1 responses include autoimmune haemolytic anaemia, autoimmune thrombocytopenic purpura, Goodpasture's syndrome, type I insulin-dependent diabetes mellitus, rheumatoid arthritis and multiple sclerosis. Disease may also ensue if a Thl-biased immune response is inappropriately directed against innocuous antigens, such as occurs in coeliac disease.
The effector mechanisms of Thl-biased immune responses include activation of macrophages that have phagocytosed microorganisms normally resistant to lysosomal destruction. Thl cytokines direct isotype switching of B-cells towards IgG production. In mice, Thl cytokines promote secretion of the opsonizing antibodies IgG2a and IgG3; in humans, the equivalent IgG subtypes are probably IgGl and IgG3. These opsonizing antibodies bind to microorganisms and promote their phagocytosis by macrophages and neutrophils, because of their affinity for phagocytes possessing Fc7 receptors and their ability to activate components of complement. Thl cytokines also mobilize and localize appropriate phagocytic cells to sites of infection. IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) promote bone-marrow stem-cell proliferation and differentiation and the generation of large numbers of phagocytes. Localization of these phagocytes to sites of infection is achieved by Thl-cell secretion of TNF-a and TNF-p and chemokines that alter the adhesive properties of local endothelial cells and act as chemotactic agents. Therefore, in an elegantly efficient, controlled and microorganism-specific manner, Thl-biased Th-cells secrete cytokines that not only promote Thl differentiation and inhibit Th2 development but also induce a complex package of biological responses directed towards the phagocytic destruction of invading microorganisms.
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