University of Texas Health Science Center at Houston, School of Public Health, Brownsville Campus, 80 Fort Brown, SPH Bldg, Brownsville, Texas 78520, USA.
Int J Infect Dis. 2011 May;15(5):e305-13. doi: 10.1016/j.ijid.2011.01.004. Epub 2011 Feb 16.
Understanding molecular immunity against mycobacterial infection is critical for the development of effective strategies to control tuberculosis (TB), which is a major health issue in the developing world. Host immunogenetic studies represent an indispensable approach to understand the molecular mechanisms against mycobacterial infection. A superb paradigm is the identification of rare mutations causing Mendelian susceptibility to mycobacterial diseases (MSMD). Mutations in the interferon-gamma (IFN-γ) receptor genes are highly specific (although not exclusive) for mycobacterial infection. Only dominant negative mutations of STAT1 have specific susceptibility to mycobacterial infection. Mutations in the interleukin-12 (IL-12) signaling genes have phenotypes with non-specificity. Current studies highlight a complex molecular network in antimycobacterial immunity, centered on IFN-γ signaling.
理解针对分枝杆菌感染的分子免疫机制对于开发控制结核病（TB）的有效策略至关重要，而结核病是发展中国家的一个主要健康问题。宿主免疫遗传学研究是理解针对分枝杆菌感染的分子机制不可或缺的方法。一个极好的范例是鉴定导致分枝杆菌疾病（MSMD）的孟德尔易感性的罕见突变。干扰素-γ（IFN-γ）受体基因的突变高度特异（尽管并非排他）于分枝杆菌感染。只有 STAT1 的显性负突变才对分枝杆菌感染具有特异性易感性。白细胞介素-12（IL-12）信号基因的突变具有非特异性表型。当前的研究强调了以 IFN-γ 信号为中心的抗分枝杆菌免疫中的复杂分子网络。
