Th17 differentiation is the default program for DPP2-deficient T-cell differentiation.
Th17 differentiation is the default program for DPP2-deficient T-cell differentiation.
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DOI:
10.1002/eji.201041157
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发表时间:
2011-06
影响因子:
5.4
通讯作者:
Huber, Brigitte T.
中科院分区:
文献类型:
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作者:
Mele, Deanna A.;Sampson, James F.;Huber, Brigitte T.
DPP2 (dipeptidyl peptidase 2) is an N-terminal dipeptidase, required for maintaining lymphocytes in a resting state. Mutant mice with T cell-specific knock-down (kd) of DPP2 (lck-DPP2 kd) were generated and analyzed for their phenotype. Normal thymocyte development and a modest increase in the proportions of peripheral T cells were observed in these mice compared to littermate controls. Interestingly, the peripheral T cells were hyperactive upon TCR stimulation in vitro, although they did not express any activation markers. Furthermore, CD3-crosslinking in the naive CD4+ and CD8+ T cells of lck-DPP2 kd mice resulted mainly in IL-17 production. Similarly, the mutant T cells secreted primarily IL-17 after in vivo priming and in vitro antigen-specific restimulation. These data suggest that IL-17 production is the default program for T cell differentiation in the absence of DPP2. Thus, DPP2 seems to impose a threshold for quiescent T cells, preventing them from drifting into cell cycle.
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影响因子:
64.5
作者:
Ivanov, Ivaylo I.;McKenzie, Brent S.;Littman, Dan R.
通讯作者:
Littman, Dan R.
DOI:
10.1084/jem.186.8.1223
发表时间:
1997-10-20
期刊:
The Journal of experimental medicine
影响因子:
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作者:
Brocker T
通讯作者:
Brocker T
影响因子:
30.5
作者:
Doreau, Agnes;Belot, Alexandre;Bonnefoy-Berard, Nathalie
通讯作者:
Bonnefoy-Berard, Nathalie
影响因子:
100.3
作者:
Dong, C
通讯作者:
Dong, C
影响因子:
30.5
作者:
通讯作者:
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