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首页> 外文期刊>Journal of interferon and cytokine research: The official journal of the International Society for Interferon and Cytokine Research >HIV alters plasma and M. tuberculosis-induced cytokine production in patients with tuberculosis.
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HIV alters plasma and M. tuberculosis-induced cytokine production in patients with tuberculosis.

机译：HIV改变了肺结核患者血浆和结核分枝杆菌诱导的细胞因子的产生。

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摘要

To test the hypothesis that HIV infection brings about an alteration in the immune response to tuberculosis (TB), mycobacterial antigen-induced production and plasma levels of the inflammatory cytokine interferon-gamma (IFN-gamma) and its regulatory cytokines interleukin-12 (IL-12), IL-18, and IL-10 were determined in patients infected dually with HIV and TB and compared with individuals with either disease and with healthy controls. Peripheral blood mononuclear cells (PBMCs) of TB patients with HIV infection produced lesser amounts of IFN-gamma and IL-12 compared with TB patients without HIV infection after in vitro stimulation with mycobacterial antigens. There was no difference in antigen-induced IL-18 production in TB patients with or without HIV infection. The in vivo cytokine pattern did not correlate with that seen in vitro. Higher levels of IFN-gamma, IL-12, and IL-18 were detected in the plasma of TB patients infected with HIV compared with TB patients without HIV infection. The presence of significantly higher plasma levels of proinflammatory cytokines suggests a greater degree of immune activation in individuals with HIV and TB, particularly those with low CD4 counts. In vitro IL-10 production by HIV-positive TB patients was similar to that of the HIV-negative TB group and higher than in HIV-positive individuals without TB, but the plasma levels were similar. HIV infection downregulates the in vitro Th1 cytokine response to TB and simultaneously increases systemic levels of these cytokines.
机译：为了检验以下假设，即艾滋病毒感染会导致对结核病（TB），分枝杆菌抗原诱导的产生和血浆中炎性细胞因子干扰素-γ（IFN-γ）及其调节性细胞因子白介素12（IL）的免疫反应发生改变-12），IL-18和IL-10是在双重感染HIV和TB的患者中测定的，并与患有任何一种疾病和健康对照的个体进行了比较。与分枝杆菌抗原进行体外刺激后，未感染HIV的结核病患者相比，感染HIV的TB患者的外周血单个核细胞（PBMC）产生的IFN-γ和IL-12较少。在有或没有HIV感染的TB患者中，抗原诱导的IL-18产生没有差异。体内细胞因子模式与体外观察到的不相关。与未感染艾滋病毒的结核病患者相比，在感染艾滋病毒的结核病患者血浆中检测到更高水平的IFN-γ，IL-12和IL-18。血浆中较高水平的促炎细胞因子的存在表明，HIV和TB患者，尤其是CD4计数低的患者，免疫活化程度更高。 HIV阳性结核病患者的体外IL-10产量与HIV阴性结核病组的相似，并且高于无结核病的HIV阳性个体，但血浆水平相似。 HIV感染会下调体外Th1细胞因子对结核病的反应，并同时增加这些细胞因子的全身水平。

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