It has recently been demonstrated that patients with systemic lupus erythematosus have a decreased number of C3B receptors on their erythrocytes. This trait is genetically determined and thus precedes and may predispose to the development of disease. It is not known how decreased erythrocyte C3b receptors participate in the pathogenesis of lupus, whether other cell types also have decreased C3b receptors, or whether inflammatory diseases such as rheumatoid arthritis, juvenile rheumatoid arthritis, and scleroderma are also associated with abnormalities of C3b receptors. Studies enumerating cellular C3b receptors by immunofluorescent flow cytometry and radioligand binding will be extended to polymorphonuclear leukocytes, monocytes, and lymphocytes to determine whether genetic control of C3b receptor number affects multiple cell types, and will focus on patients with a variety of manifestations of lupus and other inflammatory diseases, to learn how abnormalities of C3b receptors may affect the expression of inflammatory processes. Contrary to the conclusions of earlier studies, it now has been shown that a proportion of T lymphocytes have C3b receptor antigen and are able to form rosettes with bovine erythrocytes bearing C3b (Eb-C3b). It has not been established whether these T cells reside within a previously identified subset, nor have their functional capacities been determined. T cells which have C3b receptors will be purified based on their ability to form rosettes with Eb-C3b and by fluorescence-activated sorting techniques, and will be characterized according to their reactivity with monoclonal antibodies, the presence or absence on their surface of receptors for immunoglobulins, their response to mitogens, and their function in assays for helper, suppressor, natural killer, and antibody-dependent cytotoxic activities.
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