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pubmed-article:9310832pubmed:abstractTextProliferative expansion and apoptotic cell death play prominent roles in T cell development. The molecular control of cell cycle progression and apoptosis appear to be inter-connected since the Bcl-2 protein can inhibit apoptosis and slow cell cycle progression in cortical thymocytes and mature T cells, particularly during the transition from the quiescent state into the cell cycle. Here the impact of bcl-2 transgene expression on CD3-CD4-CD8- T cell progenitors was assessed. Bcl-2 enhanced the survival of these progenitors at all of the four major differentiation stages, CD25- CD44+ (pro-T1), CD25 + CD44+ (pro-T2), CD25 + CD44- (pro-T3) and CD25-CD44- (pro-T4). However, it reduced cell cycling and slowed turnover only in the pro-T4 subset. From an analysis of bcl-2 transgenic mice expressing a TCR transgene or bearing a mutation in the scid or rag-1 gene we conclude that Bcl-2 inhibits proliferation only of T cell progenitors that are activated via the pre-TCR, not those stimulated via c-Kit and the IL-7 receptor.lld:pubmed
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pubmed-article:9310832pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:9310832pubmed:articleTitlebcl-2 transgene expression promotes survival and reduces proliferation of CD3-CD4-CD8- T cell progenitors.lld:pubmed
pubmed-article:9310832pubmed:affiliationWalter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.lld:pubmed
pubmed-article:9310832pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9310832pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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