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Production of interleukin-10 and transforming growth factor beta by peripheral blood mononuclear cells in Q fever endocarditis.

机译:Q发热心内膜炎患者外周血单个核细胞产生白介素10和转化生长因子β。

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The pathophysiology of Q fever endocarditis is characterized by the suppression of antigen-specific cell-mediated immune responses. We investigated the production of interleukin-10 (IL-10) and transforming growth factor beta (TGF-beta), known to interfere with the development of protective cell immunity. IL-10 was markedly released by unstimulated peripheral blood mononuclear cells (PBMC) from patients with Q fever endocarditis. This release resulted from the upregulation of IL-10 gene transcription. Similarly, the release of TGF-beta1 and TGF-beta2 was significantly higher in patient PBMC than in control cells, but the expression of their respective mRNA was not enhanced in patient cells. In contrast, lipopolysaccharide-stimulated transcription and release of IL-10 and TGF-beta were similar in patients and controls. The release of IL-10 by PBMC but not that of TGF-beta was correlated with the clinical status of the patients. First, IL-10 production was correlated with specific antibody levels. Second, IL-10 release remained elevated in patients prone to relapse. Taken together, our results suggest that the release of IL-10 and TGF-beta is upregulated in Q fever endocarditis. IL-10 might be considered as a marker of disease relapses and might be instrumental in monitoring the efficiency of the treatment.
机译:Q热心内膜炎的病理生理学特征是抑制抗原特异性细胞介导的免疫反应。我们调查了白细胞介素10(IL-10)和转化生长因子β(TGF-β)的产生,已知这些因子会干扰保护性细胞免疫的发展。 Q型心内膜炎患者的外周血单核细胞(PBMC)不受刺激而明显释放IL-10。这种释放是由于IL-10基因转录的上调引起的。同样,患者PBMC中TGF-beta1和TGF-beta2的释放显着高于对照细胞,但其各自mRNA的表达在患者细胞中并未增强。相反,在患者和对照组中,脂多糖刺激的IL-10和TGF-β的转录和释放相似。 PBMC释放的IL-10而不是TGF-β的释放与患者的临床状况相关。首先,IL-10的产生与特异性抗体水平相关。其次,易复发患者的IL-10释放仍然较高。两者合计,我们的结果表明在Q发热心内膜炎中IL-10和TGF-β的释放上调。 IL-10可能被认为是疾病复发的标志物,并且可能在监测治疗效率中起重要作用。

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