Regulation of programmed cell death following T cell activation in vivo

International Immunology
Y YangC G Fathman

Abstract

Activation of T cell hybridomas in vitro induces rapid Fas-Fas ligand (FasL)-mediated programmed cell death (apoptosis). In contrast, T cells activated by antigen or superantigen in vivo undergo a population expansion and then decline due to Fas-FasL-mediated activation-induced apoptosis (AIA). We asked how T cells activated by antigen in vivo proliferated before undergoing apoptosis. Two possibilities were analyzed: either (i) the apoptosis program was not 'turned on' or (ii) was 'blocked' during the period of cellular proliferation in vivo. Data presented in this manuscript support the second of these possibilities. CD4+ T cells activated in vivo were resistant to anti-fas-mediated apoptosis until 48 h following staphylococcal enterotoxin B (SEB) administration, despite the fact that activated proliferating T cells expressed high levels of Fas (CD95) antigen and many 'apoptosis genes' were induced within 24 h of SEB administration. The analysis of the expression patterns of 'apoptosis genes' during the T cell activation further suggested that temporal blockade of AIA may be due to the induction of apoptosis-preventing genes, such as bag-1.

Citations

Dec 17, 2009·Bulletin of Mathematical Biology·Peter S KimDoron Levy
Oct 5, 2010·Bulletin of Mathematical Biology·Peter S KimDoron Levy
Jun 19, 2002·The Journal of Clinical Investigation·Jens V SteinMichael Hahne
Aug 7, 2013·Bulletin of Mathematical Biology·Shelby Wilson, Doron Levy
Jul 22, 2004·Journal of Neuroimmunology·Lois E McCarthyThomas J Rogers
Mar 14, 2000·The Journal of Biological Chemistry·M JenkinsJ M McCune
Mar 6, 2003·Biochimica Et Biophysica Acta·Paul A TownsendGraham Packham

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis