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发布者:鑫达医学翻译 发布时间:2012-10-31阅读:

原文
Recent data link the transcription factor T-bet, important in Th1 differentiation, with the function of Treg cells during Mtb infection and in the absence of this transcription factor Treg cells fail to persist. It is interesting that T-bet deficient mice, although more susceptible to Mtb when compared to wild-type mice, do not succumb to infection with the same kinetics as IFN-g deficient mice probably because T cells from Mtb infected T-bet deficient mice retain some capacity to produce IFN-g following in vitro stimulation. As Mtb is a strong inducer of type 1 immunity as well as IL-17-producing cells, it is possible that the absence of T-bet shifts the response to IL-17 production. Indeed, Tbet deficient mice infected with Mtb have severe inflammation as might be expected of an environment with high IL-17-producing cells. Similarly, in Trypanosoma cruzi infection it has been shown that T-bet deficient CD4 T cells develop normally and produce similar levels of IFN-g as wild-type cells however, a robust IL-17 response develops. Thus, microenvironmental factors may impair T-bet expression on a per cell basis, not significantly limiting IFN-g production per cell but enough to impact T-bet inhibition of RORgt and production of IL-17. It will be interesting to determine whether T-bet expression levels have any effect in IL-17 production by IFN-g-producing cells upon Mtb infection, and to what extent these cells are relevant to control infection or to cause immunopathological consequences. In this respect, IL-27 has been shown to induce T-bet expression in CD4 T cells and IL-27R have decreased survival and enhanced inflammation when compared to wild-type mice. It will be intriguing to determine whether this is caused by lower T-bet expression and to what extent does this affect differentiation of IL-17-producing cells.

译文
近期的一些研究将T-bet转录因子(Th1分化过程中的一类重要转录因子)与Mtb感染期间Treg功能联系起来。在缺失T-bet转录因子的情况下,Treg细胞不能充分发挥其功能。虽然T-bet缺陷小鼠对Mtb更敏感(与野生型相比),但其比γ-干扰素缺陷小鼠更具抗感染性。这可能源于T细胞仍具备产生γ-干扰素的能力。Mtb为I型免疫及IL-17产生细胞的重要诱导因子。因此,T-bet的缺失可能导致IL-17表达的改变。Mtb感染T-bet缺陷小鼠研究证实,IL-17产生细胞大量存在的条件下,小鼠更易产生恶性炎症。克鲁斯锥虫感染研究表明,T-bet缺陷CD4 T细胞发育正常,并产生与野生型相类似的γ-干扰素水平。但是小鼠IL-17应答水平增强。

因此,微环境对T-bet表达的影响可能停留在个别细胞水平,不会显著影响细胞内γ-干扰素的表达。但足以影响T-bet对RORγt的抑制及IL-17的产生过程。后续研究有必要探讨γ-干扰素产生细胞感染Mtb后T-bet是否对IL-17表达具有一定影响。此外,有必要探讨这些细胞是否与感染控制相关,及是否可导致免疫病理学病变等。 既往研究表明,IL-27可诱导CD4 T细胞内T-bet表达。与野生型相比,IL-27R可降低细胞存活率,并增强炎症反应。有必要研究该现象是否源于低剂量T-bet表达,以及该现象对IL-17分泌细胞产生怎样的影响。
 


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