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C ONTROL OF A POPTOSIS IN THE I MMUNE S YSTEM : Bcl-2, BH3-Only Proteins and More

C ONTROL OF A POPTOSIS IN THE I MMUNE S YSTEM : Bcl-2, BH3-Only Proteins and More ▪ Abstract Apoptotic cell death plays a critical role in the development and functioning of the immune system. During differentiation, apoptosis weeds out lymphocytes lacking useful antigen receptors and those expressing dangerous ones. Lymphocyte death is also involved in limiting the magnitude and duration of immune responses to infection. In this review, we describe the role of the Bcl-2 protein family, and to a lesser extent that of death receptors (members of the tumor necrosis factor receptor family with a death domain), in the control of lymphoid and myeloid cell survival. We also consider the pathogenic consequences of failure of apoptosis in the immune system. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Immunology Annual Reviews

C ONTROL OF A POPTOSIS IN THE I MMUNE S YSTEM : Bcl-2, BH3-Only Proteins and More

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References (255)

Publisher
Annual Reviews
Copyright
Copyright © 2003 by Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0732-0582
eISSN
1545-3278
DOI
10.1146/annurev.immunol.21.120601.141029
pmid
12414721
Publisher site
See Article on Publisher Site

Abstract

▪ Abstract Apoptotic cell death plays a critical role in the development and functioning of the immune system. During differentiation, apoptosis weeds out lymphocytes lacking useful antigen receptors and those expressing dangerous ones. Lymphocyte death is also involved in limiting the magnitude and duration of immune responses to infection. In this review, we describe the role of the Bcl-2 protein family, and to a lesser extent that of death receptors (members of the tumor necrosis factor receptor family with a death domain), in the control of lymphoid and myeloid cell survival. We also consider the pathogenic consequences of failure of apoptosis in the immune system.

Journal

Annual Review of ImmunologyAnnual Reviews

Published: Apr 1, 2003

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