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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >CD70 expression by dendritic cells plays a critical role in the immunogenicity of CD40-independent, CD4+ T cell-dependent, licensed CD8+ T cell responses
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CD70 expression by dendritic cells plays a critical role in the immunogenicity of CD40-independent, CD4+ T cell-dependent, licensed CD8+ T cell responses

机译：树突状细胞的CD70表达在非CD40依赖性，CD4 + T细胞依赖性，许可的CD8 + T细胞应答的免疫原性中起关键作用

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摘要

The stimulation of DC by CD4+ T cells is known to condition DC to activate na?ˉve CD8+ T cells, predominantly via CD40-CD40L interactions. It has been proposed that a critical consequence of DC conditioning is the induction of CD70 expression. Whether and how CD70 induction contributes to CD8+ T cell responses in the absence of CD40-CD40L interactions are unknown. CD8+ T cell responses to adenoviral- or DC-based immunization of CD40-deficient mice revealed a CD40-independent, CD4+ T cell-dependent pathway for CD70 induction on conventional DC. This pathway and subsequent CD8+ T cell responses were enhanced by, but not dependent on, concomitant activation of TLR and in part, used TRANCE and LIGHT/LT?±?2 stimulation. Blocking TRANCE and LIGHT/LT?±?2 during stimulation reduced the immunogenicity of CD40-deficient DC. These data support the hypothesis that induction of CD70 expression on DC after an encounter with activated CD4+ T cells is a major component of CD4+ T cell-mediated licensing of DC. Further, multiple pathways exist for CD4+ T cells to elicit CD70 expression on DC. These data in part explain the capacity of CD40-deficient mice to mount CD8+ T cell responses and may provide additional targets for immunotherapy in situations when CD40-mediated licensing is compromised.
机译：已知CD4 + T细胞对DC的刺激主要通过CD40-CD40L相互作用来调节DC激活幼稚的CD8 + T细胞。已经提出DC调节的关键结果是诱导CD70表达。在没有CD40-CD40L相互作用的情况下，CD70诱导是否以及如何促进CD8 + T细胞应答尚不清楚。 CD8 + T细胞对CD40缺陷小鼠基于腺病毒或DC的免疫反应表明，在常规DC上诱导CD70的CD40非依赖性，CD4 + T细胞依赖性途径。通过但不依赖于TLR的激活，以及不使用TRANCE和LIGHT / LT？±？2刺激，可以增强该途径和随后的CD8 + T细胞应答。在刺激过程中阻断TRANCE和LIGHT /LTα±β2会降低CD40缺陷型DC的免疫原性。这些数据支持这样的假设，即与活化的CD4 + T细胞相遇后在DC上诱导CD70表达是CD4 + T细胞介导的DC许可的主要组成部分。此外，对于CD4 + T细胞，存在多种途径引发DC上CD70的表达。这些数据部分解释了CD40缺陷型小鼠发生CD8 + T细胞反应的能力，并可能在CD40介导的许可受到损害的情况下为免疫疗法提供其他靶点。

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