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在慢性人类布鲁氏菌病中,辅助性T细胞1细胞因子产生减少与T细胞对布鲁氏菌细胞质蛋白无反应性相关。

Diminished production of T helper 1 cytokines correlates with T cell unresponsiveness to Brucella cytoplasmic proteins in chronic human brucellosis.

作者信息

Giambartolomei Guillermo H, Delpino M Victoria, Cahanovich Mariela E, Wallach Jorge C, Baldi Pablo C, Velikovsky Carlos A, Fossati Carlos A

机构信息

Instituto de Estudios de la Inmunidad Humoral, Facultad de Farmacia y Bioquímica, and Laboratorio de Inmunogenética, Hospital de Clínicas José de San Martín, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.

出版信息

J Infect Dis. 2002 Jul 15;186(2):252-9. doi: 10.1086/341449. Epub 2002 Jun 17.

Abstract

This study evaluated the cellular immune response against Brucella species cytoplasmic protein (CP) in peripheral blood mononuclear cells (PBMC) of 25 patients with brucellosis. In vitro proliferation and cytokine gene expression and production were investigated. PBMC from 14 patients proliferated in response to CP (responder patients [RPs]) and cells from 11 patients did not (nonresponder patients [NRPs]). CP-specific interleukin (IL)-2 and interferon-gamma were significantly induced in PBMC from RPs, compared with cells from NRPs. No significant differences were found in the production of IL-10 between the 2 groups. CP did not induce IL-4 production. A close relationship was observed between the clinical status of the patients and the T cell response against CP. Patient with acute infections responded to CP and induced production of T helper 1 (Th1) cytokines, whereas chronically infected patients did not. Diminished production of Th1 cytokines may contribute to T cell unresponsiveness in chronic human brucellosis.

摘要

本研究评估了25例布鲁氏菌病患者外周血单个核细胞(PBMC)中针对布鲁氏菌属细胞质蛋白(CP)的细胞免疫反应。研究了体外增殖以及细胞因子基因表达和产生情况。14例患者的PBMC对CP有增殖反应(反应者患者[RPs]),11例患者的细胞无增殖反应(无反应者患者[NRPs])。与NRPs患者的细胞相比,RPs患者的PBMC中CP特异性白细胞介素(IL)-2和干扰素-γ显著诱导产生。两组之间IL-10的产生无显著差异。CP未诱导IL-4产生。观察到患者的临床状态与针对CP的T细胞反应之间存在密切关系。急性感染患者对CP有反应并诱导产生辅助性T细胞1(Th1)细胞因子,而慢性感染患者则无反应。Th1细胞因子产生减少可能导致慢性人类布鲁氏菌病中T细胞无反应性。

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