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Bordetella pertussis Infection of Primary Human Monocytes Alters HLA-DR Expression

机译：百日咳博德特氏菌感染原代人单核细胞改变HLA-DR表达

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Bordetella pertussis is the causative agent of whooping cough, a potentially lethal respiratory disease in children. In immunocompetent individuals, B. pertussis infection elicits an effective adaptive immune response driven by activated CD4+ T cells. However, live B. pertussis persists in the host for 3 to 4 weeks prior to clearance. Thus, B. pertussis appears to have evolved short-term mechanisms for immune system evasion. We investigated the effects of B. pertussis wild-type strain BP338 on antigen presentation in primary human monocytes. BP338 infection reduced cell surface expression of HLA-DR and CD86 but not that of major histocompatibility complex class I proteins. This change in cell surface HLA-DR expression reflected intracellular redistribution of HLA-DR. The proportion of peptide-loaded molecules was unchanged in infected cells, suggesting that intracellular retention occurred after peptide loading. Although B. pertussis infection of monocytes induced rapid and robust expression of interleukin-10 (IL-10), HLA-DR redistribution did not appear to be explained by increased IL-10 levels. BP338-infected monocytes exhibited reduced synthesis of HLA-DR dimers. Interestingly, those HLA-DR proteins that were generated appeared to be longer-lived than HLA-DR in uninfected monocytes. BP338 infection also prevented gamma interferon (IFN-γ) induction of HLA-DR protein synthesis. Using mutant strains of B. pertussis, we found that reduction in HLA-DR surface expression was due in part to the presence of pertussis toxin whereas the inhibition of IFN-γ induction of HLA-DR could not be linked to any of the virulence factors tested. These data demonstrate that B. pertussis utilizes several mechanisms to modulate HLA-DR expression.
机译：百日咳博德特氏菌是百日咳的病原体，百日咳是儿童的一种致命致死性呼吸系统疾病。在具有免疫能力的个体中， B。百日咳感染引起活化的CD4 + T细胞驱动的有效适应性免疫反应。但是，直播 B。百日咳在清除前会在宿主体内持续3-4周。因此， B。百日咳似乎已发展出逃避免疫系统的短期机制。我们调查了 B的影响。百日咳野生型BP338菌株对人原代单核细胞抗原呈递的影响BP338感染会降低HLA-DR和CD86的细胞表面表达，但不能降低主要组织相容性复合I类蛋白的表达。细胞表面HLA-DR表达的这种变化反映了HLA-DR在细胞内的重新分布。肽加载的分子的比例在受感染的细胞中没有变化，这表明在肽加载后发生了细胞内保留。虽然 B。百日咳感染单核细胞会诱导白介素10（IL-10）快速而稳定地表达，HLA-DR的重新分布似乎不能由IL-10水平的升高来解释。 BP338感染的单核细胞显示出HLA-DR二聚体的合成减少。有趣的是，在未感染的单核细胞中，产生的那些HLA-DR蛋白似乎比HLA-DR寿命更长。 BP338感染还阻止了HLA-DR蛋白合成的γ干扰素（IFN-γ）诱导。使用 B的突变菌株。百日咳，我们发现HLA-DR表面表达的降低部分归因于百日咳毒素的存在，而IFN-γ诱导HLA-DR的抑制作用与测试的任何毒力因子均无关。这些数据表明 B。百日咳利用多种机制调节HLA-DR的表达。

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