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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >T Cell-Derived IL-10 Impairs Host Resistance to Mycobacterium tuberculosis Infection
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T Cell-Derived IL-10 Impairs Host Resistance to Mycobacterium tuberculosis Infection

机译：T细胞衍生的IL-10损害宿主抗结核病感染

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摘要

Tuberculosis (TB), caused by Mycobacterium tuberculosis infection, is a leading cause of mortality and morbidity, causing similar to 1.5 million deaths annually. CD4(+) T cells and several cytokines, such as the Th1 cytokine IFN-gamma, are critical in the control of this infection. Conversely, the immunosuppressive cytokine IL-10 has been shown to dampen Th1 cell responses to M. tuberculosis infection impairing bacterial clearance. However, the critical cellular source of IL-10 during M. tuberculosis infection is still unknown. Using IL-10 reporter mice, we show in this article that during the first 14 d of M. tuberculosis infection, the predominant cells expressing IL-10 in the lung were Ly6C(+) monocytes. However, after day 21 postinfection, IL-10-expressing T cells were also highly represented. Notably, mice deficient in T cell-derived IL-10, but not mice deficient in monocyte-derived IL-10, showed a significant reduction in lung bacterial loads during chronic M. tuberculosis infection compared with fully IL-10-competent mice, indicating a major role for T cell-derived IL-10 in TB susceptibility. IL-10-expressing cells were detected among both CD4(+) and CD8(+) T cells, expressed high levels of CD44 and Tbet, and were able to coproduce IFN-gamma and IL-10 upon ex vivo stimulation. Furthermore, during M. tuberculosis infection, Il10 expression in CD4(+) T cells was partially regulated by both IL-27 and type I IFN signaling. Together, our data reveal that, despite the multiple immune sources of IL-10 during M. tuberculosis infection, activated effector T cells are the major source accounting for IL-10-induced TB susceptibility.
机译：由结核病感染引起的结核病（TB）是死亡率和发病率的主要原因，每年导致类似于150万人死亡。 CD4（+）T细胞和几种细胞因子，例如Th1细胞因子IFN-Gamma对该感染的控制至关重要。相反，免疫抑制细胞因子IL-10已被证明抑制了对M.结核病感染损害细菌间隙的细胞反应。然而，M.结核病感染期间IL-10的临界细胞来源仍然未知。使用IL-10报告小鼠，我们在本文中展示了在肺部结核感染的前14d中，在肺中表达IL-10的主要细胞是LY6C（+）单核细胞。然而，在第21天发射后，表达IL-10表达的T细胞也具有高度代表。值得注意的是，缺乏T细胞衍生的IL-10的小鼠，但不是单核细胞衍生的IL-10缺乏小鼠，其与完全IL-10主管小鼠相比，慢性M.结核病感染期间肺细菌载荷显着降低TB易感性T细胞衍生IL-10的主要作用。在CD4（+）和CD8（+）T细胞中检测IL-10表达细胞，表达高水平的CD44和TBET，并且能够在离体刺激后共同促进IFN-Gamma和IL-10。此外，在结核病感染期间，CD4（+）T细胞中的IL10表达由IL-27和I型IFN信号传导部分调节。我们的数据一起揭示了，尽管在结核病感染期间IL-10的多种免疫来源，但活性效应效应T细胞是IL-10诱导的TB易感性的主要源核算。

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