Bergman Molly A, Cummings Lisa A, Barrett Sara L Rassoulian, Smith Kelly D, Lara J Cano, Aderem Alan, Cookson Brad T
Department of Laboratory Medicine and Microbiology, University of Washington Medical Center, Mailstop 357110, 1959 NE Pacific Ave., Seattle, WA 98195, USA.
Infect Immun. 2005 Mar;73(3):1350-6. doi: 10.1128/IAI.73.3.1350-1356.2005.
A better understanding of immunity to infection is revealed from the characteristics of microbial ligands recognized by host immune responses. Murine infection with the intracellular bacterium Salmonella generates CD4+ T cells that specifically recognize Salmonella proteins expressed in bacterial surface organelles such as flagella and membrane vesicles. These natural Salmonella antigens are also ligands for Toll-like receptors (TLRs) or avidly associated with TLR ligands such as lipopolysaccharide (LPS). PhoP/PhoQ, a regulon controlling Salmonella virulence and remodeling of LPS to resist innate immunity, coordinately represses production of surface-exposed antigens recognized by CD4+ T cells and TLRs. These data suggest that genetically coordinated surface modifications may provide a growth advantage for Salmonella in host tissues by limiting both innate and adaptive immune recognition.
从宿主免疫反应所识别的微生物配体特征中,可以更好地理解对感染的免疫。用细胞内细菌沙门氏菌感染小鼠会产生CD4+ T细胞,这些细胞特异性识别在细菌表面细胞器(如鞭毛和膜泡)中表达的沙门氏菌蛋白。这些天然沙门氏菌抗原也是Toll样受体(TLR)的配体,或者与TLR配体(如脂多糖(LPS))紧密相关。PhoP/PhoQ是一个调控沙门氏菌毒力和LPS重塑以抵抗先天免疫的调节子,它协同抑制CD4+ T细胞和TLR所识别的表面暴露抗原的产生。这些数据表明,通过限制先天免疫和适应性免疫识别,基因协调的表面修饰可能为沙门氏菌在宿主组织中提供生长优势。