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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Perturbation of the CD4 T cell compartment and expansion of regulatory T cells in autoimmune-prone Lyn-deficient mice.
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Perturbation of the CD4 T cell compartment and expansion of regulatory T cells in autoimmune-prone Lyn-deficient mice.

机译：CD4 T细胞区室的扰动和自身免疫易发Lyn缺陷小鼠中调节性T细胞的扩增。

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摘要

Regulatory T cells (Tregs) are a subset of T lymphocytes that are responsible for suppressing the function of other immune cells, and preventing potentially harmful autoimmune responses. Studies in autoimmune-prone mice and human autoimmune diseases have shown reduced Treg number or function as a causative factor for the apparent loss of tolerance that contributes to disease. We have found that Lyn-deficient mice, which develop high titers of autoantibodies with age, have a perturbed Treg compartment. Contrary to what has been observed in some strains of autoimmune-prone mice, aged Lyn-deficient mice have increased numbers of Tregs. This expansion occurs in the presence of elevated serum IL-2 and diminished TGF-beta. Despite expansion of the Treg compartment, Lyn-deficient mice succumb at approximately 1 year of age due to immune complex-mediated glomerulonephritis. We have shown that Lyn is not expressed in Tregs or indeed in any T cell subset, suggesting that the expansion and apparent functional deficiency in Tregs in Lyn-deficient mice is due to extrinsic factors rather than an intrinsic Treg defect. Indeed, using an in vivo colitis model, we have shown that Lyn-deficient Tregs can suppress inflammation. These results suggest that Tregs are expanding in Lyn-deficient mice in an effort to control the autoimmune disease but are simply overwhelmed by the disease process. This study highlights the role of the inflammatory setting in autoimmune disease and its consideration when contemplating the use of Tregs as an autoimmune therapy.
机译：调节性T细胞（Tregs）是T淋巴细胞的子集，负责抑制其他免疫细胞的功能，并防止潜在的有害自身免疫反应。对易患自身免疫性小鼠和人类自身免疫性疾病的研究表明，Treg数量减少或作为导致疾病明显丧失耐受力的病因。我们发现，Lyn缺陷小鼠随着年龄的增长会产生高滴度的自身抗体，它们的Treg区室受到干扰。与某些自身免疫易感小鼠品系相反，年老的Lyn缺陷小鼠的Treg数量增加。在血清IL-2升高和TGF-β降低的情况下发生这种扩增。尽管Treg区室扩大，但由于免疫复合物介导的肾小球肾炎，Lyn缺陷小鼠在大约1岁时屈服。我们已经显示，Lyn在Tregs或任何T细胞亚群中均未表达，这表明Lyn缺陷小鼠中Tregs的扩增和表观功能缺陷是由于外在因素而非固有的Treg缺陷所致。确实，使用体内结肠炎模型，我们已经证明Lyn缺乏的Treg可以抑制炎症。这些结果表明，Tregs在Lyn缺陷小鼠中正在扩大，以努力控制自身免疫性疾病，但被疾病过程所淹没。这项研究突出了炎症环境在自身免疫性疾病中的作用及其在考虑使用Tregs作为自身免疫疗法时的考虑因素。

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