摘要
本文旨在通过观察结核分枝杆菌刺激后巨噬细胞抗原呈递功能的变化, 探讨结核分枝杆菌的免疫逃逸机制。在体外, 结核分枝杆菌刺激巨噬细胞24 h 后, 用流式细胞仪检测γ干扰素( IFN-γ) 诱导的主要组织相容性复合物( MHC) Ⅱ类分子、CD86 和CD80 的表达变化; 酶联免疫吸附试验( ELISA) 检测巨噬细胞的抗原呈递功能; 反转录-聚合酶链反应检测巨噬细胞CⅡTA 及其启动子PⅠ、PⅢ和PⅣ的mRNA 水平。结果发现, 结核分枝杆菌抑制IFN-γ诱导的巨噬细胞表面MHCⅡ 类分子和CD86 的表达, 且呈剂量依赖性, 但CD80的表达变化不明显; 抗原呈递功能明显降低; 结核分枝杆菌刺激后巨细胞CⅡTA 及其启动子PⅠ、PⅢ和PⅣ的mRNA 水平显著降低。提示结核分枝杆菌可能通过降低CⅡTA 及其启动子PⅠ、PⅢ和PⅣ 的mRNA 水平, 抑制IFN-γ诱导的巨噬细胞MHCⅡ类分子的表达; 结核分枝杆菌可降低巨噬细胞CD86 的表达, 抑制IFN-γ诱导的巨噬细胞抗原呈递功能。
Abstract
The present study was aimed to investigate major histocompatibility complex Ⅱ ( MHC Ⅱ ) antigen presentation induced by interferon-γ ( IFN-γ) in macrophages after exposure to Mycobacterium tuberculosis ( M. uberculosis) . The expressions of MHCⅡ, CD86, and CD80 on macrophages, after exposure to M. tuberculosis for 24 h prior to the addition of IFN-γ, were detected by flow cytometry. The mRNA levels of CⅡTA, PⅠ, PⅢ and PⅣ were assayed by reverse transcriptase-polymerase chain reaction. MHCⅡ antigen presentation was detected by enzyme-linked immunosorbent assay ( ELISA) . The results showed that M. tuberculosis inhibited the expressions of MHCⅡ and CD86 but not CD80 induced by IFN-γon macrophages. The ability of antigen presentation was also inhibited. The mRNA levels of CⅡTA, PⅠ, PⅢ and PⅣ induced by IFN-γwere also decreased. It suggests that M. tuberculosis inhibits MHCⅡ antigen presentation induced by IFN-γon macrophages.
关键词
抗原呈递 /
γ干扰素
Key words
Mycobacterium tuberculosis /
Antigen presentation /
Interferon-γ
王翠妮；徐薇；熊思东.
结核分枝杆菌对巨噬细胞抗原呈递功能的抑制作用[J]. 微生物与感染. 2009, 4(3): 132-136
WANG Cui-Ni；XU Wei；XIONG Si-Dong.
Mycobacterium tuberculosis inhibits antigen presentation in
macrophages[J]. Journal of Microbes and Infections. 2009, 4(3): 132-136
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