Saiga Hiroyuki, Shimada Yosuke, Takeda Kiyoshi
Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka, Japan.
Clin Dev Immunol. 2011;2011:347594. doi: 10.1155/2011/347594. Epub 2011 Jan 12.
Tuberculosis, which is caused by infection with Mycobacterium tuberculosis (Mtb), remains one of the major bacterial infections worldwide. Host defense against Mtb is mediated by a combination of innate and adaptive immune responses. In the last 15 years, the mechanisms for activation of innate immunity have been elucidated. Toll-like receptors (TLRs) have been revealed to be critical for the recognition of pathogenic microorganisms including mycobacteria. Subsequent studies further revealed that NOD-like receptors and C-type lectin receptors are responsible for the TLR-independent recognition of mycobacteria. Several molecules, such as active vitamin D(3), secretary leukocyte protease inhibitor, and lipocalin 2, all of which are induced by TLR stimulation, have been shown to direct innate immune responses to mycobacteria. In addition, Irgm1-dependent autophagy has recently been demonstrated to eliminate intracellular mycobacteria. Thus, our understanding of the mechanisms for the innate immune response to mycobacteria is developing.
由结核分枝杆菌（Mtb）感染引起的结核病仍然是全球主要的细菌感染之一。宿主对Mtb的防御由先天性和适应性免疫反应共同介导。在过去15年中，先天性免疫激活的机制已被阐明。Toll样受体（TLR）已被证明对包括分枝杆菌在内的致病微生物的识别至关重要。随后的研究进一步表明，NOD样受体和C型凝集素受体负责对分枝杆菌的非TLR依赖性识别。几种分子，如活性维生素D(3)、分泌型白细胞蛋白酶抑制剂和脂质运载蛋白2，均由TLR刺激诱导产生，已被证明可引导对分枝杆菌的先天性免疫反应。此外，最近已证明Irgm1依赖性自噬可清除细胞内的分枝杆菌。因此，我们对分枝杆菌先天性免疫反应机制的理解正在不断发展。
