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Cell death is a common event during B cell development. The demise of developing B cells is a regulated process that serves to select cell populations bearing functional receptors and to remove cells that are no longer needed or potentially autoreactive. Bcl-2 and Bcl-XL, two members of the bcl-2 gene family of programmed cell death regulators with anti-apoptotic activity, are expressed in a highly regulated pattern during B cell maturation. Overexpression of Bcl-2 in developing B cells of transgenic mice, in the presence of T cell dependent costimulatory signals, results in the generation of a modified B cell repertoire and in the production of pathogenic autoantibodies. While disregulation of programmed cell death in B cells may cause autoimmune manifestations in mice, the involvement of such alterations in the pathogenesis of autoimmune diseases in humans merits further investigation.

Citation

M López-Hoyos, R Carrió, J Merino, R Merino. Regulation of B cell apoptosis by Bcl-2 and Bcl-XL and its role in the development of autoimmune diseases (Review). International journal of molecular medicine. 1998 Feb;1(2):475-83

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PMID: 9852253

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