Interleukin-2 rescues helpless effector CD8+ T cells by diminishing the susceptibility to TRAIL mediated death.
Interleukin-2 rescues helpless effector CD8+ T cells by diminishing the susceptibility to TRAIL mediated death.
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DOI：
10.1016/j.imlet.2011.04.011
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发表时间：
2011-09-30
影响因子：
4.4
通讯作者：
Janssen, Edith M.
中科院分区：
文献类型：
--
作者：
Wolkers, Monika C.;Bensinger, Steven J.;Green, Douglas R.;Schoenberger, Stephen P.;Janssen, Edith M.
CD8+ T cells primed in the absence of CD4+ T cell help are programmed to produce TRAIL, which results in Death receptor (DR5) mediated apoptosis upon restimulation. Here, we studied whether these `helpless' effector CD8+ T cells are consigned to an apoptotic fate or whether their helpless program can be altered by inflammatory or growth cytokines. We found that helpless CD8+ T cells regained their full proliferative and functional capacity only when IL-2 was added to cell cultures, while IL-7 and IL-15, two common gamma chain cytokines associated with CD8+ T cell homeostasis and memory, could only partly restore secondary expansion in helpless CD8+ T cells. Recovery of functional CD8+ T cell immunity by IL-2 was concomitant with induction of IL2Rα (CD25) expression, downregulation of TRAIL, and the upregulation of anti-apoptotic molecules Bcl-2 and FLIP. The addition of IL-2 to helpless CD8+ T cells also interfered with DR5-mediated apoptosis induction, indicating that IL-2 affects several components of the TRAIL-DR5 pathway. Collectively, these data demonstrate that the helpless phenotype is not fixed, and that IL-2R signaling at the time of reactivation can play an important role in restoring CD8+ T cell function.
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影响因子：
15.3
作者：
Takeda, K;Yamaguchi, N;Smyth, MJ
通讯作者：
Smyth, MJ
影响因子：
30.5
作者：
Badovinac, VP;Porter, BB;Harty, JT
通讯作者：
Harty, JT
影响因子：
2.2
作者：
McDermott, David F.;Atkins, Michael B.
通讯作者：
Atkins, Michael B.
在体内对Epstein-Barr病毒的主要免疫反应期间，抗原特异性CD8+ T细胞的直接可视化。
DOI：
10.1084/jem.187.9.1395
发表时间：
1998-05-04
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Callan MF;Tan L;Annels N;Ogg GS;Wilson JD;O'Callaghan CA;Steven N;McMichael AJ;Rickinson AB
通讯作者：
Rickinson AB
影响因子：
30.5
作者：
Kaech, SM;Ahmed, R
通讯作者：
Ahmed, R