CD8(+) T cells sabotage their own memory potential through IFN-γ-dependent modification of the IL-12/IL-15 receptor α axis on dendritic cells.
CD8(+) T cells sabotage their own memory potential through IFN-γ-dependent modification of the IL-12/IL-15 receptor α axis on dendritic cells.
复制标题
DOI：
10.4049/jimmunol.1101580
复制
发表时间：
2012-04-15
期刊：
影响因子：
--
通讯作者：
Guevara-Patiño JA
中科院分区：
文献类型：
--
作者：
Kohlhapp FJ;Zloza A;O'Sullivan JA;Moore TV;Lacek AT;Jagoda MC;McCracken J;Cole DJ;Guevara-Patiño JA
CD8+T细胞反应受树突状细胞(DC)和CD4+T细胞的调节，导致CD8+T细胞在自身分化过程中起被动作用。相反，通过使用DNA疫苗模型，我们证明了CD8+T细胞本身通过依赖CD8+T细胞衍生的干扰素γ修饰DC上的IL-12/IL-15Rα轴来主动限制自身的记忆能力。这种由CD8+T细胞驱动的细胞因子变化导致T-bet升高和Bcl2表达降低，从而减少记忆祖细胞的形成。这些结果证实了CD8+T细胞在调节自身效应器分化命运中的未知作用，以及炎症和记忆形成之间的平衡关系。
CD8+ T cell responses have been shown to be regulated by dendritic cells (DCs) and CD4+ T cells leading to the tenet that CD8+ T cells play a passive role in their own differentiation. In contrast, by using a DNA vaccination model, to separate the events of vaccination from those of CD8+ T cell priming, we demonstrate that CD8+ T cells, themselves, actively limit their own memory potential through CD8+ T cell-derived IFN-γ-dependent modification of the IL-12/IL-15Rα axis on DCs. Such CD8+ T cell-driven cytokine alterations result in increased T-bet and decreased Bcl-2 expression, and thus decreased memory progenitor formation. These results identify an unrecognized role for CD8+ T cells in the regulation of their own effector differentiation fate and a previously uncharacterized relationship between the balance of inflammation and memory formation.
登录
查看更多内容
影响因子：
20.3
作者：
Nakahara, Takeshi;Uchi, Hiroshi;Houghton, Alan N.
通讯作者：
Houghton, Alan N.
影响因子：
32.4
作者：
Mortier, Erwan;Advincula, Rommel;Ma, Averil
通讯作者：
Ma, Averil
影响因子：
4.4
作者：
Min, Lin;Isa, Siti Aminah Bte Mohammad;Ruedl, Christiane
通讯作者：
Ruedl, Christiane
影响因子：
30.5
作者：
Intlekofer, AM;Takemoto, N;Reiner, SL
通讯作者：
Reiner, SL
影响因子：
30.5
作者：
Badovinac, VP;Porter, BB;Harty, JT
通讯作者：
Harty, JT