The control of apoptosis in lymphocyte selection
Details
Publication Year 2003-06,Volume 193,Issue #1,Page 82-92
Journal Title
IMMUNOLOGICAL REVIEWS
Publication Type
Journal Article
Abstract
The stochastic nature of rearrangement and diversification of the gene segments encoding immunoglobulins (Igs) and T cell receptors (TCRs) inevitably gives rise to immature B and T lymphocytes that lack antigen receptors or express useless or dangerous (self-antigen-specific) ones. Signaling through antigen receptors promotes survival, proliferative expansion and further differentiation of useful cells and deletion of the useless and dangerous ones. During immune responses, pathogen-specific B and T lymphocytes, as well as cells of the innate immune system, undergo extensive proliferation and develop effector functions, such as antibody secretion, cytotoxicity or cytokine production. To prevent tissue damage by these effector molecules, activated lymphocytes are removed when an infection has been overcome. Together with other mechanisms, including developmental arrest and induction of unresponsiveness (anergy), programmed cell death (apoptosis) of autoreactive lymphocytes safeguards immunological tolerance to self and assists in the development of an effective immune system. We have been investigating the molecular mechanisms that control programmed cell death. This review describes some of our experiments using transgenic and knockout mice, which overexpress or lack apoptosis regulators, that led to discoveries on how life and death decisions are made during development and functioning of the immune system.
Publisher
BLACKWELL MUNKSGAARD
Keywords
T-CELL-RECEPTOR; BCL-2 FAMILY MEMBERS; DOMINANT INTERFERING MUTANT; TRANSGENIC MICE; FAS-LIGAND; B-CELLS; DEFICIENT MICE; AUTOREACTIVE THYMOCYTES; NEGATIVE SELECTION; CLONAL ELIMINATION
Terms of Use/Rights Notice
Refer to copyright notice on published article.


Creation Date: 2003-06-01 12:00:00
An error has occurred. This application may no longer respond until reloaded. Reload 🗙