Bcl-x and the regulation of survival in the immune system.
A variety of experimental models indicate that programmed cell death, or apoptosis, of lymphocytes is a key mechanism in the homeostatic regulation of immunity. Apoptosis is important in early B- and T-cell development to delete cells with nonfunctional antigen receptors, and is also critical for censoring self-reactive cells at the immature lymphocyte stage and at various stages after lymphocytes reach maturity. In this article we focus on the role of the apoptosis regulatory gene bcl-x in controlling survival during lymphocyte development and following B- and T-cell activation. Interesting parallels are observed for bcl-x expression between the B- and T-lineages. The available data also indicate that bcl-x and bcl-2 are expressed in reciprocal patterns during the lifespan of a lymphocyte, suggesting unique regulatory roles for these two survival proteins.
Behrens
T W
TW
Center for Immunology, University of Minnesota Medical School, Minneapolis 55455, USA. behre001@maroon.tc.umn.edu
Mueller
D L
DL
D000276:Adjuvants, Immunologic / Q000502:physiology*; D000818:Animals; D002454:Cell Differentiation / Q000235:genetics / Q000276:immunology; D002470:Cell Survival / Q000235:genetics / Q000276:immunology; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D007107:Immune System / Q000166:cytology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology*; D051020:bcl-X Protein
D000276:Adjuvants, Immunologic; C494811:BCL2L1 protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D051020:bcl-X Protein