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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >An atypical CD8 T-cell response to Chlamydia muridarum genital tract infections includes T cells that produce interleukin-13
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An atypical CD8 T-cell response to Chlamydia muridarum genital tract infections includes T cells that produce interleukin-13

机译：对鼠衣原体生殖道感染的非典型CD8 T细胞反应包括产生白介素13的T细胞

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摘要

Chlamydia trachomatis urogenital serovars D-K are intracellular bacterial pathogens that replicate almost exclusively in human reproductive tract epithelium. In the C. muridarum mouse model for human Chlamydia genital tract infections CD4 T helper type 1 cell responses mediate protective immunity while CD8 T-cell responses have been associated with scarring and infertility. Scarring mediated by CD8 T cells requires production of tumour necrosis factor-α (TNF-α); however, TNF-α is associated with protective immunity mediated by CD4 T cells. The latter result suggests that TNF-α in-and-of itself may not be the sole determining factor in immunopathology. CD8 T cells mediating immunopathology presumably do something in addition to producing TNF-α that is detrimental during resolution of genital tract infections. To investigate the mechanism underlying CD8 immunopathology we attempted to isolate Chlamydia-specific CD8 T-cell clones from mice that self-cleared genital tract infections. They could not be derived with antigen-pulsed irradiated naive splenocytes; instead derivation required use of irradiated immune splenocyte antigen-presenting cells. The Chlamydia-specific CD8 T-cell clones had relatively low cell surface CD8 levels and the majority were not restricted by MHC class Ia molecules. They did not express Plac8, and had varying abilities to terminate Chlamydia replication in epithelial cells. Two of the five CD8 clones produced interleukin-13 (IL-13) in addition to IL-2, TNF-α, IL-10 and interferon-γ. IL-13-producing Chlamydia-specific CD8 T cells may contribute to immunopathology during C. muridarum genital tract infections based on known roles of TNF-α and IL-13 in scar formation.
机译：沙眼衣原体泌尿生殖道血清D-K是细胞内细菌病原体，几乎仅在人的生殖道上皮中复制。在人类衣原体生殖道感染的mur。C. muridarum小鼠模型中，CD4 T辅助细胞1型细胞应答介导保护性免疫，而CD8 T细胞应答与瘢痕形成和不育症相关。 CD8 T细胞介导的瘢痕形成需要产生肿瘤坏死因子-α（TNF-α）。然而，TNF-α与CD4 T细胞介导的保护性免疫有关。后一个结果表明，TNF-α本身可能不是免疫病理学的唯一决定因素。介导免疫病理学的CD8 T细胞可能除了产生TNF-α以外还可以做一些事情，而TNF-α在解决生殖道感染时是有害的。为了研究潜在的CD8免疫病理学机制，我们试图从自清除生殖道感染的小鼠中分离出衣原体特异性CD8 T细胞克隆。它们不能由抗原脉冲辐照的幼稚脾细胞衍生;取而代之，需要使用辐照的免疫脾细胞抗原呈递细胞。衣原体特异性CD8 T细胞克隆具有相对较低的细胞表面CD8水平，并且大多数不受I类MHC分子的限制。它们不表达Plac8，并且具有终止上皮细胞中衣原体复制的能力。除IL-2，TNF-α，IL-10和干扰素-γ外，五个CD8克隆中的两个还产生白介素13（IL-13）。产生IL-13的衣原体特异性CD8 T细胞可能基于已知的TNF-α和IL-13在瘢痕形成中的作用而参与了衣原体生殖道感染期间的免疫病理学研究。

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