Pathogen-induced inflammatory environment controls effector and memory CD8+ T cell differentiation.
Pathogen-induced inflammatory environment controls effector and memory CD8+ T cell differentiation.
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DOI:
10.4049/jimmunol.1102335
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发表时间:
2011-11-15
期刊:
影响因子:
--
通讯作者:
Lefrançois L
中科院分区:
文献类型:
--
作者:
Obar JJ;Jellison ER;Sheridan BS;Blair DA;Pham QM;Zickovich JM;Lefrançois L
In response to infection CD8+ T cells integrate multiple signals and undergo an exponential increase in cell numbers. Simultaneously, a dynamic differentiation process occurs, resulting in the formation of short-lived (SLEC; CD127lowKLRG1high) and memory-precursor (MPEC; CD127highKLRG1low) effector cells from an early-effector cell (EEC) that is CD127lowKLRG1low in phenotype. CD8+ T cell differentiation during vesicular stomatitis virus (VSV) infection differed significantly than during Listeria monocytogenes infection with a substantial reduction in EEC differentiation into SLECs. SLEC generationwas dependent on Ebi3 expression. Furthermore, SLEC differentiation during VSV infection wasenhanced by administration ofCpG-DNA, through an IL-12 dependent mechanism. Moreover, CpG-DNAtreatment enhanced effector CD8+ T cell functionality and memory subset distribution, but in an IL-12 independent manner. Population dynamics were dramatically different during secondary CD8+ T cell responses, with a much greater accumulation of SLECs and the appearance of a significant number of CD127highKLRG1highmemory cells, both of which were intrinsic to the memory CD8+ T cell. These subsets persisted for several months, but were less effective in recall than MPECs. Thus, our data shed light on how varying the context of T cell priming alters downstream effector and memory CD8+ T cell differentiation.
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DOI:
10.1084/jem.20052237
发表时间:
2006-04-17
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
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通讯作者:
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影响因子:
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通讯作者:
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影响因子:
30.5
作者:
Intlekofer, AM;Takemoto, N;Reiner, SL
通讯作者:
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