Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 201, Issue 4, Pages 603-614Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20041924
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Funding
- NCI NIH HHS [P30 CA021765, CA-21765] Funding Source: Medline
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The pre-T cell receptor (TCR) is expressed early during T cell development and imposes a tight selection for differentiating T cell progenitors. Pre-TCR-expressing cells are selected to survive and differentiate further, whereas pre-TCR- cells are negatively selected to die. The mechanisms of pre-TCR-mediated survival are poorly understood. Here, we describe the induction of the antiapoptotic gene BCL2A1 (A1) as a potential mechanism regulating inhibition of pre-T cell death. We characterize in detail the signaling pathway involved in A1 induction and show that A1 expression can induce pre-T cell survival by inhibiting activation of caspase-3. Moreover, we show that in vitro knockdown of A1 expression can compromise survival even in the presence of a functional pre-TCR. Finally, we suggest that pre-TCR-induced A1 overexpression can contribute to T cell leukemia in both mice and humans.
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