Compensatory dendritic cell development mediated by BATF-IRF interactions.
Compensatory dendritic cell development mediated by BATF-IRF interactions.
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AP-1转录因子Batf 3是CD 8 α+经典树突状细胞稳态发育所必需的，该树突状细胞引发针对细胞内病原体的CD 8 T细胞应答。在这里，我们确定了一种替代的，Batf 3独立的途径，其发展过程中的细胞因子IL-12和IFN-γ介导的细胞内病原体感染的操作。这种替代途径是由相关AP-1因子Batf（也在T和B细胞中起作用）提供的Batf 3的分子补偿和细胞因子响应感染诱导的Batf 2引起的。反过来，Batf和Batf 3之间的生理补偿也发生在T细胞中以表达IL-10和CTLA-4。BATF因子之间的补偿是基于它们的亮氨酸拉链结构域与非AP-1因子如Irf 4和Irf 8相互作用以介导协同基因激活的共享能力。可以想象，操纵树突状细胞发育的这种替代途径可能在增强对疫苗的免疫应答方面具有价值。
The AP-1 transcription factor Batf3 is required for homeostatic development of CD8α+ classical dendritic cells that prime CD8 T-cell responses against intracellular pathogens. Here, we identify an alternative, Batf3-independent pathway for their development operating during infection with intracellular pathogens mediated by the cytokines IL-12 and IFN-γ. This alternative pathway results from molecular compensation for Batf3 provided by the related AP-1 factors Batf, which also functions in T and B cells, and Batf2 induced by cytokines in response to infection. Reciprocally, physiologic compensation between Batf and Batf3 also occurs in T cells for expression of IL-10 and CTLA-4. Compensation among BATF factors is based on the shared capacity of their leucine zipper domains to interact with non-AP-1 factors such as Irf4 and Irf8 to mediate cooperative gene activation. Conceivably, manipulating this alternative pathway of dendritic cell development could be of value in augmenting immune responses to vaccines.
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DOI：
10.1073/pnas.011404098
发表时间：
2001-01-02
影响因子：
11.1
作者：
Li, C;Wong, WH
通讯作者：
Wong, WH
影响因子：
3.7
作者：
Edelson BT;Bradstreet TR;KC W;Hildner K;Herzog JW;Sim J;Russell JH;Murphy TL;Unanue ER;Murphy KM
通讯作者：
Murphy KM
影响因子：
11.4
作者：
Brass, AL;Zhu, AQ;Singh, H
通讯作者：
Singh, H
DOI：
10.1084/jem.192.12.1685
发表时间：
2000-12-18
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
den Haan JM;Lehar SM;Bevan MJ
通讯作者：
Bevan MJ
影响因子：
32.4
作者：
Gorman, JR;vanderStoep, N;Alt, FW
通讯作者：
Alt, FW