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首页> 外文期刊>The Journal of Infectious Diseases >Mycobacterium tuberculosis-Induced Reduction of Interferon {gamma}-Producing CD4 T cells in active tuberculosis.
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Mycobacterium tuberculosis-Induced Reduction of Interferon {gamma}-Producing CD4 T cells in active tuberculosis.

机译:结核分枝杆菌诱导的活动性结核病中产生干扰素{γ}的CD4 T细胞的还原。

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To the Editor-A recent study by Streitz et al [1] demonstrated a higher frequency of tuberculin-specific CD4 T cells carrying activation markers in peripheral blood of individuals with latent Mycobacterium tuberculosis infection than in those with active pulmonary tuberculosis. As an explanation, the authors suggested that activated T cells may migrate to infected tissues. They left unexplained the fact that more interferon (IFN) gamma-producing T cells (T-helper 1 [Th1] cells) were found in patients with latent M. tuberculosis infection than in those with active pulmonary tuberculosis [1]. Authors of recent studies into the immunopathology of active tuberculosis described 2 main mechanisms for reduced Thl cells in active pulmonary tuberculosis; the main one seems to be an M. tuberculosis-induced increase in immunosuppressive cytokines and in-tracellular mechanisms. One study quantified lung immune mediator gene expression in cells obtained from induced sputum of patients with active pulmonary tuberculosis; compared with controls, these patients had significantly higher levels of mediators that may impair Th1 immunity (interleukin [IL] 10, transforming growth factor-betaRII, interleukin-1 receptor-associated kinase (IRAK)-M, IL-IRn, suppressor of cyto-kine signaling (SOCS) 1, SOCS3, and indoleamine 2,3-dioxygenase (IDO) [2].
机译:致编辑-Streitz等人[1]的最新研究表明,潜伏性结核分枝杆菌感染者外周血中带有激活标记的结核菌素特异性CD4 T细胞的频率高于活动性肺结核患者。作为一种解释,作者建议活化的T细胞可能会迁移到受感染的组织。他们无法解释的事实是,潜在的结核分枝杆菌感染患者比活动性肺结核患者发现更多的产生干扰素(IFN)的T细胞(T辅助1 [Th1]细胞)。关于活动性肺结核免疫病理学的最新研究的作者描述了减少活动性肺结核中Th1细胞减少的2种主要机制。主要的原因似乎是结核分枝杆菌诱导的免疫抑制细胞因子和细胞内机制的增加。一项研究量化了活动性肺结核患者的痰液中获得的细胞中肺免疫介质基因的表达。与对照组相比,这些患者的介体水平明显升高,可能会损害Th1免疫力(白介素[IL] 10,转化生长因子-βRII,白介素-1受体相关激酶(IRAK)-M,IL-IRn,细胞抑制剂) -Kine信号(SOCS)1,SOCS3和吲哚胺2,3-二加氧酶(IDO)[2]。

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