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首页> 外文期刊>Molecular medicine. >Genetic regulation of T regulatory, CD4, and CD8 cell numbers by the arthritis severity loci Cia5a, Cia5d, and the MHC/Cia1 in the rat.
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Genetic regulation of T regulatory, CD4, and CD8 cell numbers by the arthritis severity loci Cia5a, Cia5d, and the MHC/Cia1 in the rat.

机译：大鼠关节炎严重程度基因座Cia5a，Cia5d和MHC / Cia1对T调节，CD4和CD8细胞数量的遗传调节。

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摘要

T cells have a central role in the pathogenesis of autoimmune arthritis, and several abnormalities in T cell homeostasis have been described in rheumatoid arthritis (RA). We hypothesized that T cell phenotypes, including frequencies of different subsets of T regulatory (Treg) cells and in vitro functional responses could be genetically determined. Furthermore, we considered that the genetic contribution would be accounted for by one of the arthritis regulatory quantitative trait loci (QTL), thus providing novel clues to gene mode of action. T cells were isolated from thymus, peripheral blood, and spleen from DA (arthritis-susceptible) and ACI and F344 (arthritis-resistant) strains and from F344.DA(Cia1), DA.F344(Cia5a), and DA.F344(Cia5d) rats congenic for arthritis QTL. T cell subpopulations differed significantly between DA, F344, and ACI. DA rats had an increased frequency of CD4(+) cells, and a reduction in CD8(+) and CD4(+)CD45RC(|o) Treg cells, compared with F344. The differences in CD4/CD8 and CD4(+)CD45RC(|o) Treg cells were accounted for by Cia5a. DA rats also had a reduced frequency of CD8(+)CD45RC(|o) CD25(+) Treg cells compared with F344, and that difference was explained by Cia5d. DA rats also had a significantly lower frequency of CD4(+)CD25(+) and CD8(+)CD25(+) thymocytes, and of peripheral blood CD8(+)CD45RC(|o) Treg cells, compared with F344 rats, and that difference was accounted for by the MHC. This is the first identification of arthritis severity QTL regulating numbers of CD4(+)CD45RC(|o) (Cia5a) and CD8(+)CD45RC(|o) CD25(+) (Cia5d) Treg cells. The MHC effect on CD8(+) Treg cells and CD25(+) thymocytes raises a novel potential explanation for its association with arthritis.
机译：T细胞在自身免疫性关节炎的发病机理中具有重要作用，并且在类风湿性关节炎（RA）中已描述了T细胞稳态的一些异常情况。我们假设可以通过遗传方法确定T细胞表型，包括T调节（Treg）细胞不同亚群的频率和体外功能反应。此外，我们认为遗传贡献将由关节炎调节定量性状基因座（QTL）之一解释，从而为基因作用方式提供了新的线索。 T细胞从胸腺，外周血和脾脏中分离出来，分别来自DA（易感关节炎），ACI和F344（抗关节炎）菌株以及F344.DA（Cia1），DA.F344（Cia5a）和DA.F344（ Cia5d）大鼠因关节炎而产生QTL。在DA，F344和ACI之间，T细胞亚群存在显着差异。与F344相比，DA大鼠的CD4（+）细胞频率增加，CD8（+）和CD4（+）CD45RC（| o）Treg细胞减少。 Cia5a解释了CD4 / CD8和CD4（+）CD45RC（| o）Treg细胞的差异。与F344相比，DA大鼠的CD8（+）CD45RC（| o）CD25（+）Treg细胞频率也降低，而这种差异由Cia5d解释。与F344大鼠相比，DA大鼠的CD4（+）CD25（+）和CD8（+）CD25（+）胸腺细胞以及外周血CD8（+）CD45RC（| o）Treg细胞的频率也显着降低。 MHC解释了这一差异。这是关节炎严重性QTL调控CD4（+）CD45RC（| o）（Cia5a）和CD8（+）CD45RC（| o）CD25（+）（Cia5d）Treg细胞数量的首次鉴定。 MHC对CD8（+）Treg细胞和CD25（+）胸腺细胞的影响为它与关节炎的联系提出了一种新的潜在解释。

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