Fully functional memory CD8 T cells in the absence of CD4 T cells
Fully functional memory CD8 T cells in the absence of CD4 T cells
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DOI：
10.4049/jimmunol.173.2.969
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发表时间：
2004-07-15
影响因子：
4.4
通讯作者：
Lefrançois, L
中科院分区：
文献类型：
--
作者：
Marzo, AL;Vezys, V;Lefrançois, L
CD 4 T细胞在感染的初级和次级反应中为CD 8 T细胞提供帮助的作用仍然存在争议。利用表达相同抗原的病毒和细菌的重组菌株，我们确定了在水泡性口炎病毒和单核细胞增生李斯特菌（LM）感染的内源性CD 8 T细胞应答中对CD 4 T细胞的需求。CD 4 T细胞的耗竭对淋巴组织或非淋巴组织中原发性或继发性水泡性口炎病毒特异性CD 8 T细胞的频率没有影响。相反，初级LM特异性CD 8 T细胞应答是CD 4 T细胞依赖性的。令人惊讶的是，LM特异性CD 8 T细胞回忆应答也是CD 4 T细胞依赖性的，这与CD 40/CD 40 L相互作用的需要相关。然而，同时抑制CD 40 L和CD 4 T细胞的清除表明，这些途径可能是独立运作的。重要的是，尽管在回忆反应期间或整个反应过程中没有CD 4 T细胞，但CD 8记忆T细胞是功能性效应子，并且与它们的“帮助”对应物等同地增殖。这些数据质疑的论点，CD 4 T细胞的条件记忆CD 8 T细胞在初级反应，并表明，在感染后产生的CD 8记忆细胞的CD 4 T细胞的主要作用是通过共刺激信号的增殖或生存的增强。
The role of CD4 T cells in providing help to CD8 T cells in primary and secondary responses to infection remains controversial. Using recombinant strains of virus and bacteria expressing the same Ag, we determined the requirement for CD4 T cells in endogenous CD8 T cell responses to infection with vesicular stomatitis virus And Listeria monocytogenes (LM). Depletion of CD4 T cells had no effect on the frequency of primary or secondary vesicular stomatitis virus-specific CD8 T cells in either lymphoid or nonlymphoid tissues. In contrast, the primary LM-specific CD8 T cell response was CD4 T cell dependent. Surprisingly, the LM-specific CD8 T cell recall response was also CD4 T cell dependent, which correlated with a requirement for CD40/CD40L interactions. However, concomitant inhibition of CD40L and CD4 T cell removal revealed that these pathways may be operating independently. Importantly, despite the absence of CD4 T cells during the recall response or throughout the entire response, CD8 memory T cells were functional effectors and proliferated equivalently to their "helped" counterparts. These data call into question the contention that CD4 T cells condition memory CD8 T cells during the primary response and indicate that the principal role of CD4 T cells in generating CD8 memory cells after infection is augmentation of proliferation or survival through costimulatory signals.