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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Association of CD4+ CD25+ T Cells with Prevention of Severe Destructive Arthritis in Borrelia burgdorferi-Vaccinated and Challenged Gamma Interferon-Deficient Mice Treated with Anti-Interleukin-17 Antibody
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Association of CD4+ CD25+ T Cells with Prevention of Severe Destructive Arthritis in Borrelia burgdorferi-Vaccinated and Challenged Gamma Interferon-Deficient Mice Treated with Anti-Interleukin-17 Antibody

机译：CD4 + CD25 + T细胞与预防抗白细胞介素17抗体治疗的伯氏疏螺旋体疫苗和挑战性γ干扰素缺陷小鼠中的严重破坏性关节炎的关系

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CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-γ°) C57BL/6 mice challenged with the Lyme spirochete. When B. burgdorferi-vaccinated and challenged IFN-γ° mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. Furthermore, histopathologic examination showed the mice to be free of destructive arthritis. When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. More importantly, severe destructive arthropathy was induced. In addition, delayed administration of anti-CD25 antibody decreased the severity of the arthritis. These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi.
机译：CD4 + CD25 + T细胞是负责主动抑制自身免疫的调节性T细胞群体。具体而言，已显示CD4 + CD25 + T细胞可预防胰岛素依赖型糖尿病，炎症性肠病和胰腺炎。在这里，我们提供的证据表明CD4 + CD25 + T细胞在控制接种博氏疏螺旋体的细菌的严重性中也起着重要作用γ干扰素缺陷（IFN-γ°）C57BL / 6小鼠用莱姆螺旋体攻击。当 B。用抗白细胞介素17（IL-17）抗体处理已接种博格多夫菌且经攻击的IFN-γ°小鼠，CD4 + CD25 + T细胞在局部淋巴结中增加。此外，组织病理学检查显示小鼠没有破坏性关节炎。当这些抗IL-17治疗的 B。注射了burgdorferi 疫苗的小鼠和攻击小鼠也接受了抗CD25抗体，局部淋巴结中的CD4 + CD25 + T细胞数量减少。更重要的是，诱发了严重的破坏性关节病。另外，抗CD25抗体的延迟给药降低了关节炎的严重性。这些结果表明，CD4 + CD25 + T细胞参与了由疫苗接种和 B攻击实验模型诱导的严重破坏性关节炎的调节。 burgdorferi 。

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