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首页> 外文期刊>Cellular immunology >H-2 alleles contribute to antigen 85-specific interferon-gamma responses during Mycobacterium tuberculosis infection.
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H-2 alleles contribute to antigen 85-specific interferon-gamma responses during Mycobacterium tuberculosis infection.

机译:H-2等位基因在结核分枝杆菌感染期间有助于抗原85特异性干扰素-γ反应。

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摘要

The in vitro immune responses to mycobacterial antigens have been linked to the H-2 loci in mice. We evaluated in vitro and in vivo immune responses during early Mycobacterium tuberculosis (M.tb) pulmonary infection of C57BL/6 (H-2(b)), C57BL/6 (H-2(k)), CBA/J (H-2(k)), and C3H/HeJ (H-2(k)) mice to determine H-2(k)-dependent and -independent effects. H-2(k)-dependent effects included delayed and diminished Ag85-specific Th1 cell priming, a reduced frequency of Ag85-specific IFN-gamma producing cells, reduced IFN-gamma protein in vivo, and increased M.tb lung burden as demonstrated by C57BL/6 H-2(k) mice vs. C57BL/6 mice. H-2(k)-independent factors controlled the amount of Ag85-specific IFN-gamma produced by each cell, T cell numbers, granuloma size, and lymphocytic infiltrates in the lungs. Overall, these results suggest that an H-2(k)-dependent suboptimal generation of Ag85-specific cells impairs control of early M.tb growth in the lungs. H-2(k)-independent factors influence the potency of IFN-gamma producing cells and immune cell trafficking during pulmonary M.tb infection.
机译:对分枝杆菌抗原的体外免疫反应已与小鼠的H-2基因座相关。我们评估了早期结核分枝杆菌(M.tb)肺部感染C57BL / 6(H-2(b)),C57BL / 6(H-2(k)),CBA / J(H -2(k))和C3H / HeJ(H-2(k))小鼠,以确定H-2(k)依赖性和非依赖性效应。 H-2(k)依赖的作用包括延迟和减少Ag85特异性Th1细胞的启动,减少Ag85特异性IFN-γ产生细胞的频率,体内IFN-γ蛋白的减少以及M.tb肺负荷的增加C57BL / 6 H-2(k)小鼠对C57BL / 6小鼠的影响。 H-2(k)独立因子控制着每个细胞产生的Ag85特异性IFN-γ的数量,T细胞数量,肉芽肿大小和肺中的淋巴细胞浸润。总体而言,这些结果表明,H-2(k)依赖的亚最佳Ag85特异性细胞的生成损害了肺中早期M.tb生长的控制。 H-2(k)独立的因素影响肺结核分枝杆菌感染期间产生IFN-γ的细胞的效力和免疫细胞的运输。

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