Inhibition of major histocompatibility complex II expression and antigen processing in murine alveolar macrophages by Mycobacterium bovis BCG and the 19-kilodalton mycobacterial lipoprotein
Inhibition of major histocompatibility complex II expression and antigen processing in murine alveolar macrophages by Mycobacterium bovis BCG and the 19-kilodalton mycobacterial lipoprotein
复制标题
DOI：
10.1128/iai.72.4.2101-2110.2004
复制
发表时间：
2004-04-01
影响因子：
3.1
通讯作者：
Boom, WH
中科院分区：
文献类型：
--
作者：
Fulton, SA;Reba, SM;Boom, WH
肺泡巨噬细胞是抵抗结核分枝杆菌的主要防御系统，但它们不能控制结核分枝杆菌。没有获得性T细胞免疫的结核病。本研究确定了小鼠肺泡巨噬细胞的抗原呈递细胞功能和模型分枝杆菌（Mycobacterium bovis BCG）对其进行调节的能力。大多数（80 - 85%）肺泡巨噬细胞同时表达CD 80（B7.1）和CD 11 c，20 - 30%共表达主要组织相容性复合物II（MHC-II）。γ干扰素（IFN-γ）增强MHC-II，但不B7.1表达。未处理或IFN-γ处理的肺泡巨噬细胞不表达CD 86（B7.2）、CD 11b、Mac-3、CD 40或F4/80。M.牛BCG和19 kDa分枝杆菌脂蛋白抑制IFN-γ调节的肺泡巨噬细胞MHC-II表达，抑制依赖于Toll样受体2。19 kDa脂蛋白对MHC-II表达的抑制与可溶性抗原向T细胞的呈递减少有关。因此，结核病的易感性可能是由于分枝杆菌干扰肺泡巨噬细胞的MHC-II表达和抗原呈递的能力。
Alveolar macrophages constitute a primary defense against Mycobacterium tuberculosis, but they are unable to control M. tuberculosis without acquired T-cell immunity. This study determined the antigen-presenting cell function of murine alveolar macrophages and the ability of the model mycobacterium, Mycobacterium bovis BCG, to modulate it. The majority (80 to 85%) of alveolar macrophages expressed both CD80 (B7.1) and CD11c, and 20 to 30% coexpressed major histocompatibility complex II (MHC-II). Gamma interferon (IFN-gamma) enhanced MHC-II but not B7.1 expression. Naive or IFN-gamma-treated alveolar macrophages did not express CD86 (B7.2), CD11b, Mac-3, CD40, or F4/80. M. bovis BCG and the 19-kDa mycobacterial lipoprotein inhibited IFN-gamma-regulated MHC-II expression on alveolar macrophages, and inhibition was dependent on Toll-like receptor 2. The inhibition of MHC-II expression by the 19-kDa lipoprotein was associated with decreased presentation of soluble antigen to T cells. Thus, susceptibility to tuberculosis may result from the ability of mycobacteria to interfere with MHC-II expression and antigen presentation by alveolar macrophages.