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非洲蜱咬热患者的细胞因子谱和 T 细胞反应。

Inflammatory cytokine profile and T cell responses in African tick bite fever patients.

机构信息

Bernhard Nocht Institute for Tropical Medicine, Bernhard-Nocht-Str. 74, 20359, Hamburg, Germany.

University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

出版信息

Med Microbiol Immunol. 2022 Jun;211(2-3):143-152. doi: 10.1007/s00430-022-00738-5. Epub 2022 May 11.

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

非洲蜱咬热是一种急性发热性疾病,由专性细胞内细菌立克次体引起。到目前为止,针对立克次体感染的免疫反应主要在体外通过受感染的内皮细胞作为主要靶细胞进行了研究,并在小鼠模型中进行了研究。患者研究很少,对于人类感染的免疫学知之甚少。在这项研究中,在聚合酶链反应确认的 R. africae 感染的 13 名患者的样本中,在疾病的不同时间点检查了炎症介质和 T 细胞反应。Th1 相关细胞因子 IFNγ 和 IL-12 在疾病的急性期增加,T 细胞趋化因子 CXCL-10 的水平也增加。此外,抗炎细胞因子 IL-10 和 IL-22 也升高。在疾病过程中,CD4 和 CD8 T 细胞越来越多地产生 IL-22,但不是 IFNγ。除 IFNγ外,IL-22似乎对立克次体感染具有保护作用。

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