![]() One of the first identified mechanisms of action of intravenous immunoglobulin was blockade of Fcγ receptors on macrophages, thereby inhibiting platelet phagocytosis in idiopathic thrombocytopenic purpura. Ab = antibody, B = B cell, CTL = cytotoxic T cell, DC = dendritic cell, FcγR = Fcγ receptor, IFN = interferon, IL = interleukin, Mo = monocyte, MΦ = macrophage, NK = natural killer cell, Pl = plasma cell, Th = T helper cell, Treg = regulatory T cell. Orange antibody structures = intravenous immunoglobulin dark grey arrows = activation signalling red arrows = agonist effect of intravenous immunoglobulin red T bars = inhibitory effect of intravenous immunoglobulin. ![]() Intravenous immunoglobulin interacts with various cellular and soluble components of the immune system involved in the inflammatory and autoimmune process: (1) it neutralizes pathogenic autoantibodies through the anti-idiotypic network (2) it modulates the expression of Fc receptors and inhibits the maturation and activation of antigen-presenting cells (3) it regulates antibody synthesis and the B-cell repertoire (4) it shifts the balance between subsets of T helper cells and downregulates the production of pro-inflammatory cytokines by T cells (5) it blocks antibody-dependent cell-mediated cytotoxicity and (6) it blocks complement activation. T helper cells and innate cells provide activation signals through cytokines, which leads either to production of autoantibodies from the differentiated B cells into plasma cells or to tissue damage from the release of inflammatory mediators by immune cells, complement activation and antibody-dependent cell-mediated cytotoxicity. ![]() Exposure of autoantigens triggers the recognition by antigen-presenting cells, leading to activation and polarization of T helper cells. Impact of intravenous immunoglobulin on the immune system.
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