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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 naive 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/LTalphabeta stimulation. Blocking TRANCE and LIGHT/LTalphabeta 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以激活幼稚的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。 CD40（-）T细胞对基于CD40缺陷小鼠的腺病毒或DC免疫的反应显示，常规DC上CD70诱导的CD40独立，CD4（+）T细胞依赖途径。该途径和随后的CD8（+）T细胞反应通过但不依赖于TLR的同时激活而得到增强，并且部分依赖于TRANCE和LIGHT / LTalphabeta刺激。在刺激过程中阻断TRANCE和LIGHT / LTalphabeta降低了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，DC上CD70表达的诱导是CD4（+）T细胞介导的DC许可的主要组成部分。此外，CD4（+）T细胞存在多种途径，以引起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目标。

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