Abstract：
African tick bite fever, an acute febrile illness, is caused by the obligate intracellular bacterium Rickettsia africae. Immune responses to rickettsial infections have so far mainly been investigated in vitro with infected endothelial cells as the main target cells, and in mouse models. Patient studies are rare and little is known about the immunology of human infections. In this study, inflammatory mediators and T cell responses were examined in samples from 13 patients with polymerase chain reaction-confirmed R. africae infections at different time points of illness. The Th1-associated cytokines IFNγ and IL-12 were increased in the acute phase of illness, as were levels of the T cell chemoattractant cytokine CXCL-10. In addition, the anti-inflammatory cytokine IL-10 and also IL-22 were elevated. IL-22 but not IFNγ was increasingly produced by CD4+ and CD8+ T cells during illness. Besides IFNγ, IL-22 appears to play a protective role in rickettsial infections.
摘要：
非洲蜱叮咬热，急性发热性疾病,是由专性细胞内细菌非洲立克次体引起的。到目前为止，对立克次体感染的免疫反应主要是以感染的内皮细胞为主要靶细胞的体外研究，和老鼠模型。患者研究很少，对人类感染的免疫学知之甚少。在这项研究中,我们在13例聚合酶链反应证实的非洲R.Africae感染患者的不同发病时间点的样本中检测了炎症介质和T细胞反应.Th1相关的细胞因子IFNγ和IL-12在疾病的急性期增加，T细胞趋化因子CXCL-10的水平。此外,抗炎细胞因子IL-10和IL-22升高。在疾病期间，CD4+和CD8+T细胞越来越多地产生IL-22而不是IFNγ。除了IFNγ，IL-22似乎在立克次体感染中起保护作用。
