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首页> 外文期刊>Infection and immunity >Regulation of Human CD4+ αβ T-Cell-Receptor-Positive (TCR+) and γδ TCR+ T-Cell Responses to Mycobacterium tuberculosis by Interleukin-10 and Transforming Growth Factor β
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Regulation of Human CD4+ αβ T-Cell-Receptor-Positive (TCR+) and γδ TCR+ T-Cell Responses to Mycobacterium tuberculosis by Interleukin-10 and Transforming Growth Factor β

机译：白细胞介素10和转化生长因子β对人CD4 +αβT细胞受体阳性（TCR +）和γδTCR + T细胞对结核分枝杆菌反应的调节

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Mycobacterium tuberculosis is the etiologic agent of human tuberculosis and is estimated to infect one-third of the world's population. Control of M. tuberculosis requires T cells and macrophages. T-cell function is modulated by the cytokine environment, which in mycobacterial infection is a balance of proinflammatory (interleukin-1 [IL-1], IL-6, IL-8, IL-12, and tumor necrosis factor alpha) and inhibitory (IL-10 and transforming growth factor β [TGF-β]) cytokines. IL-10 and TGF-β are produced by M. tuberculosis-infected macrophages. The effect of IL-10 and TGF-β on M. tuberculosis-reactive human CD4+and γδ T cells, the two major human T-cell subsets activated byM. tuberculosis, was investigated. Both IL-10 and TGF-β inhibited proliferation and gamma interferon production by CD4+ and γδ T cells. IL-10 was a more potent inhibitor than TGF-β for both T-cell subsets. Combinations of IL-10 and TGF-β did not result in additive or synergistic inhibition. IL-10 inhibited γδ and CD4+ T cells directly and inhibited monocyte antigen-presenting cell (APC) function for CD4+ T cells and, to a lesser extent, for γδ T cells. TGF-β inhibited both CD4+ and γδ T cells directly and had little effect on APC function for γδ and CD4+ T cells. IL-10 down-regulated major histocompatibility complex (MHC) class I, MHC class II, CD40, B7-1, and B7-2 expression on M. tuberculosis-infected monocytes to a greater extent than TGF-β. Neither cytokine affected the uptake of M. tuberculosis by monocytes. Thus, IL-10 and TGF-β both inhibited CD4+ and γδ T cells but differed in the mechanism used to inhibit T-cell responses to M. tuberculosis.
机译：结核分枝杆菌是人类结核病的病原体，据估计感染了世界三分之一的人口。 M的控制。结核病需要T细胞和巨噬细胞。 T细胞功能受细胞因子环境的调节，这种环境在分枝杆菌感染中是促炎（白介素-1 [IL-1]，IL-6，IL-8，IL-12和肿瘤坏死因子α）和抑制因子之间的平衡。 （IL-10和转化生长因子β[TGF-β]）细胞因子。 IL-10和TGF-β由 M生产。结核感染的巨噬细胞。 IL-10和TGF-β对 M的影响。结核病反应性人CD4 + 和γδT细胞，是 M激活的两个主要人T细胞亚群。对结核病进行了调查。 IL-10和TGF-β均抑制CD4 + 和γδT细胞的增殖和γ干扰素的产生。对于两个T细胞亚群，IL-10均比TGF-β更有效。 IL-10和TGF-β的组合不会导致累加或协同抑制作用。 IL-10直接抑制γδ和CD4 + T细胞，并抑制CD4 + T细胞（在较小程度上）对δδ的单核细胞抗原呈递细胞（APC）的功能。 T细胞。 TGF-β直接抑制CD4 + 和γδT细胞，对γδ和CD4 + T细胞的APC功能影响很小。 IL-10下调M上的主要组织相容性复合体（MHC）I类，MHC II类，CD40，B7-1和B7-2表达。结核病感染的单核细胞比TGF-β感染的程度更大。两种细胞因子均不影响 M的摄取。单核细胞感染结核病。因此，IL-10和TGF-β均抑制CD4 + 和γδT细胞，但在抑制T细胞对 M反应的机制上有所不同。结核病。

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