曼氏血吸虫感染诱导1型CD8+细胞应答。

Behring Institute Mitteilungen Pub Date : 1997-03-01
E J Pearce, J Pedras-Vasconcelos
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引用次数: 0

摘要

我们已经发现,感染大型细胞外寄生虫S. mansoni导致1型CD8+ T细胞反应的发展。虽然这种免疫反应有许多鲜为人知的方面,但我们的工作假设是,它的功能主要是调节寄生虫卵抗原诱导的Th2反应,而Th2反应本身负责环周肉芽肿的形成。这种关于CD8+细胞活性的观点反映了Bloom及其同事的假设,即2型CD8+细胞的功能是调节Th1反应。既然我们已经认识到Th1和Th2细胞可以相互交叉调节,为什么在血吸虫病期间,要使用1型CD8+而不是Th1应答来调节Th2应答呢?这个问题的部分答案可能在于1型CD8+细胞对IL-4的明显依赖。正因为如此,ifn - γ(一种潜在危险的促炎细胞因子)的过量产生的可能性很小,只有在需要时才提供“抑制”。Th1细胞在ifn - γ的产生上不依赖于IL-4。目前实验室的工作是为了检验这里提出的各种假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Schistosoma mansoni infection induces a type 1 CD8+ cell response.

We have found that infection with the large extracellular parasite S. mansoni leads to the development of a type 1 CD8+ T cell response. While there are many poorly understood aspects of this immune response, our working hypothesis is that it functions primarily to regulate the parasite egg-antigen induced Th2 response, which itself is responsible for circumoval granunuloma formation. This view of the activity of CD8+ cells mirrors Bloom and colleagues' postulate that type 2 CD8+ cells function to regulate Th1 responses. Since it is well recognized that Th1 and Th2 cells can cross regulate each other, why should a type 1 CD8+ rather than a Th1 response be used for the regulation of the Th2 response during schistosomiasis? The answer to this may in part lie in the apparent dependence of the type 1 CD8+ cells on IL-4. Because of this, there is little likelihood for the over-production of IFN-gamma (a potentially dangerous proinflammatory cytokine) and "suppression" is provided only when needed. Th1 cells have no such dependence on IL-4 for IFN-gamma production. Current work in the laboratory is directed towards testing the various hypotheses put forward here.

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