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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Neutrophil-dependent tumor rejection and priming of tumoricidal CD8+ T cell response induced by dendritic cells overexpressing CD95L.
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Neutrophil-dependent tumor rejection and priming of tumoricidal CD8+ T cell response induced by dendritic cells overexpressing CD95L.

机译：中性粒细胞依赖性肿瘤排斥反应和由过表达CD95L的树突状细胞诱导的杀肿瘤CD8 + T细胞反应的启动。

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摘要

Overexpression of CD95 (Fas/Apo-1) ligand (CD95L) has been shown to induce T cell tolerance but also, neutrophilic inflammation and rejection of allogeneic tissue. We explored the capacity of dendritic cells (DCs) genetically engineered to overexpress CD95L to induce an antitumor response. We first found that DCs overexpressing CD95L, in addition to MHC class I-restricted OVA peptides (CD95L-OVA-DCs), induced increased antigen-specific CD8(+) T cell responses as compared with DCs overexpressing OVA peptides alone. The enhanced T cell responses were associated with improved regression of a tumor expressing OVA, allowing survival of all animals. When DCs overexpressing CD95L (CD95L-DCs) were injected with the tumor expressing OVA, in vivo tumor proliferation was strikingly inhibited. A strong cellular apoptosis and a massive neutrophilic infiltrate developed in this setting. Neutrophil depletion prevented tumor regression as well as enhanced IFN-gamma production induced by CD95L-OVA-DCs. Furthermore, theCD8(+) T cell response induced by the coadministration of tumor cells and CD95L-DCs led to rejection of a tumor implanted at a distance from the DC injection site. In summary, DCs expressing CD95L promote tumor rejection involving neutrophil-mediated innate immunity and CD8(+) T cell-dependent adaptative immune responses.
机译：CD95（Fas / Apo-1）配体（CD95L）的过表达已显示出诱导T细胞耐受性，但也诱导中性粒细胞炎症和异体组织排斥。我们探讨了基因工程改造过表达CD95L诱导诱导抗肿瘤反应的树突状细胞（DC）的能力。我们首先发现，与I类MHC限制型OVA肽（CD95L-OVA-DCs）相比，DCs过表达CD95L诱导的抗原特异性CD8（+）T细胞应答与单独过表达DC的DCs相比增加。增强的T细胞反应与表达OVA的肿瘤的消退改善有关，从而允许所有动物存活。当向过表达CD95L的DC（CD95L-DC）注射表达OVA的肿瘤时，体内肿瘤的增殖会受到明显抑制。在这种情况下发生了强烈的细胞凋亡和大量嗜中性粒细胞浸润。中性粒细胞耗竭可以防止肿瘤消退以及CD95L-OVA-DCs诱导的IFN-γ产生增加。此外，由肿瘤细胞和CD95L-DC共同给药诱导的CD8（+）T细胞反应导致排斥在距DC注射部位一定距离处植入的肿瘤。总之，表达CD95L的DC促进肿瘤排斥反应，涉及中性粒细胞介导的先天免疫和CD8（+）T细胞依赖性适应性免疫应答。

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