Abstract

The fate of B lymphocytes is dependent on intrinsic and B cell antigen receptor (BCR) induced signals. These signals are modified and interpreted by other cell-surface molecules such as CD19 and CD22 that govern mature B cell activation. This review assesses our current understanding of how CD19 and CD22 regulate B lymphocyte signaling and how alterations in these response-regulators contribute to autoimmunity in mice and humans. We propose that CD19 functions as a specialized adapter protein that regulates B lymphocyte signaling and autoantibody production. Overexpression of CD19 by B cells in systemic sclerosis patients correlates with autoantibody production and transgenic mice that overexpress CD19 produce similar autltoantibodies. CD19 establishes a novel Src-family kinase activation loop that reguates basal signal transduction thresholds in resting B cells and amplifes Src-family kinase activation following BCR Iigation. Reciprocally, CD22 is a potent regulator of CD19 function. These observations provide insight into how CD19 and CD22 govern the molecular ordering and intensity of signals transduced in B cells that may contribute to autoimmunity. (Keio J Med 49 (1): l-13, March 2000)

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