Regulation of B cell apoptosis by Bcl-2 and Bcl-XL and its role in the development of autoimmune diseases (Review).
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.
López-Hoyos
M
M
Servicio de Inmunologia, Hospital Universitario Marques de Valdecilla, Spain.
Carrió
R
R
Merino
J
J
Merino
R
R
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D001327:Autoimmune Diseases / Q000276:immunology*; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology*; D002451:Cell Compartmentation; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology; D051379:Mice; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000276:immunology*; D051020:bcl-X Protein
C494811:BCL2L1 protein, human; C494812:Bcl2l1 protein, mouse; D019253:Proto-Oncogene Proteins c-bcl-2; D051020:bcl-X Protein