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前沿:小鼠莱姆病中T细胞介导的病理学

Cutting edge: T cell-mediated pathology in murine Lyme borreliosis.

作者信息

McKisic M D, Redmond W L, Barthold S W

机构信息

Center for Comparative Medicine, University of California, Davis 95616, USA.

出版信息

J Immunol. 2000 Jun 15;164(12):6096-9. doi: 10.4049/jimmunol.164.12.6096.

Abstract

Even in the absence of an appropriate model or direct evidence, T cells have been hypothesized to exacerbate the manifestations of Lyme disease. To define definitely the role of T cells in Lyme disease, the course of disease in immunocompetent and B cell-deficient mice was compared. By 8 wk postinoculation, immunocompetent mice resolved both carditis and arthritis, whereas foci of myocarditis and severe destructive arthritis characterized disease of B cell-deficient mice. Cell transfer experiments using infected B6-Rag1 knock out mice demonstrated that: 1) innate immunity mediated the initial sequelae of infection, 2) transferring both naive T cells and B cells induced resolution of carditis and arthritis, 3) infected mice reconstituted with T cells developed myocarditis and severe destructive arthritis, and 4) CD4+ T cells were responsible for the observed immune-mediated pathology. These data demonstrate directly the deleterious effect of T cells in Lyme disease.

摘要

即使在缺乏合适模型或直接证据的情况下,也有假说认为T细胞会加剧莱姆病的症状。为明确T细胞在莱姆病中的作用,对免疫功能正常和B细胞缺陷小鼠的病程进行了比较。接种后8周,免疫功能正常的小鼠的心脏炎和关节炎均得到缓解,而B细胞缺陷小鼠的疾病特征为心肌炎病灶和严重的破坏性关节炎。使用感染的B6-Rag1基因敲除小鼠进行的细胞转移实验表明:1)天然免疫介导了感染的初始后遗症;2)同时转移幼稚T细胞和B细胞可诱导心脏炎和关节炎的缓解;3)用T细胞重建的感染小鼠出现了心肌炎和严重的破坏性关节炎;4)CD4+T细胞导致了所观察到的免疫介导病理。这些数据直接证明了T细胞在莱姆病中的有害作用。

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