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Yan Wang and Noel Rose Background: The complement system is made up of a series of about 25 proteins that work to "complement" the activity of antibodies in destroying bacteria, either by facilitating phagocytosis or by puncturing the bacterial cell membrane. Complement also helps to rid the body of antigen-antibody complexes. In carrying out these tasks, it induces an inflammatory response. Complement proteins circulate in the blood in an inactive form. When the first of the complement substances is triggered-usually by antibody interlocked with an antigen-it sets in motion ripple effect. As each component is activated in turn, it acts upon the next in a precise sequence of carefully regulated steps known as the "complement cascade." Advance: Myocarditis is a principal cause of heart disease among young adults and it often foretells heart failure. Advanced forms of myocarditis are characterized by the presence of autoantibodies and T cells. These investigators report that complement is critical for the induction of autoimmune myocarditis in a laboratory mouse model, and that it acts through complement receptors Type 1 and 2 (CR1 and CR2). They also found a subset of T cells that express CR1 and CR2 and propose that both receptors are necessary for the expression of B and T cell activation markers, T cell proliferation, and cytokine production. Implication: These findings describe the mechanism by which complement, a key product of the normal immune system, affects the development of autoimmune disease. This finding may have significant impact on the development of therapeutic approaches for the treatment of human autoimmune disease. Citation: Kaya Z, Afanasyeva M, Wang Y, Dohmen KM, Schlichting J, Tretter T, Fairweather D, Holers VM, Rose NR. Contribution of the innate immune system to autoimmune myocarditis: a role for complement. Nat Immunol. 2001 Aug;2(8):739-45. |
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