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在副球孢子菌病患者的疾病活动期,γ干扰素的产生受损,而在临床缓解后恢复。

Production of IFN-gamma is impaired in patients with paracoccidioidomycosis during active disease and is restored after clinical remission.

作者信息

Karhawi A S, Colombo A L, Salomão R

机构信息

Division of Infectious Diseases, Universidade Federal de São Paulo, Clementino, Brazil.

出版信息

Med Mycol. 2000 Jun;38(3):225-9. doi: 10.1080/mmy.38.3.225.229.

Abstract

Cellular immunity is usually suppressed during paracoccidioidomycosis (PCM) and is restored after treatment. In this study we evaluated the induction of a type 1 (interferon gamma (IFN-gamma)), a type 2 (interleukin (IL)-10) and a primarily macrophage derived cytokine (tumor necrosis factor (TNF)-alpha) in peripheral blood mononuclear cells (PBMC) from patients with PCM. Eight male patients with active PCM, nine male patients with clinical remission of the disease and 10 healthy control subjects were enrolled in the study. Cytokines were induced with non-specific stimuli --phytohaemagglutin (PHA) (induces IL-10 and IFN-gamma), Lipopolysaccharide (induces TNF-alpha)--and Paracoccidioides brasiliensis antigen (PbAg) (induces IL-10, IFN-gamma and TNF-alpha). Induction of IFN-gamma with PHA differed among the three groups (P < 0.01; Kruskal-Wallis test) and with PbAg was lower in patients with active disease compared to those in clinical remission (P = 0.05; Mann-Whitney). Induction of IL-10 and of TNF-alpha was similar in the three groups. The suppressed production of IFN-gamma in patients with active disease may underscore the cellular immune deficiency seen in these patients.

摘要

细胞免疫在副球孢子菌病(PCM)期间通常受到抑制,治疗后恢复。在本研究中,我们评估了PCM患者外周血单个核细胞(PBMC)中1型(干扰素γ(IFN-γ))、2型(白细胞介素(IL)-10)和主要由巨噬细胞衍生的细胞因子(肿瘤坏死因子(TNF)-α)的诱导情况。8名患有活动性PCM的男性患者、9名临床缓解的男性患者和10名健康对照者参与了本研究。细胞因子通过非特异性刺激物诱导——植物血凝素(PHA)(诱导IL-10和IFN-γ)、脂多糖(诱导TNF-α)——以及巴西副球孢子菌抗原(PbAg)(诱导IL-10、IFN-γ和TNF-α)。三组之间PHA诱导IFN-γ的情况不同(P < 0.01;Kruskal-Wallis检验),与临床缓解患者相比,活动性疾病患者中PbAg诱导IFN-γ的水平较低(P = 0.05;Mann-Whitney检验)。三组中IL-10和TNF-α的诱导情况相似。活动性疾病患者中IFN-γ产生的抑制可能突出了这些患者中存在的细胞免疫缺陷。

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