Nandi Bisweswar, Chatterjee Madhumouli, Hogle Kathryn, McLaughlin Maura, MacNamara Katherine, Racine Rachael, Winslow Gary M
Wadsworth Center, New York State Department of Health, 120 New Scotland Ave., Albany, NY 12208, USA.
Infect Immun. 2009 Oct;77(10):4643-53. doi: 10.1128/IAI.01433-08. Epub 2009 Jul 27.
How spatial and temporal changes in major histocompatibility complex/peptide antigen presentation to CD4 T cells regulate CD4 T-cell responses during intracellular bacterial infections is relatively unexplored. We have shown that immunization with an ehrlichial outer membrane protein, OMP-19, protects mice against fatal ehrlichial challenge infection, and we identified a CD4 T-cell epitope (IA(b)/OMP-19(107-122)) that elicited CD4 T cells following either immunization or infection. Here, we have used an IA(b)/OMP-19(107-122)-specific T-cell line to monitor antigen display ex vivo during acute and chronic infection with Ehrlichia muris, a bacterium that establishes persistent infection in C57BL/6 mice. The display of IA(b)/OMP-19(107-122) by host antigen-presenting cells was detected by measuring intracellular gamma interferon (IFN-gamma) production by the T-cell line. After intravenous infection, antigen presentation was detected in the spleen, peritoneal exudate cells, and lymph nodes, although the kinetics of antigen display differed among the tissues. Antigen presentation and bacterial colonization were closely linked in each anatomical location, and there was a direct relationship between antigen display and CD4 T-cell effector function. Spleen and lymph node dendritic cells (DCs) were efficient presenters of IA(b)/OMP-19(107-122), demonstrating that DCs play an important role in ehrlichial infection and immunity. Chronic infection and antigen presentation occurred within the peritoneal cavity, even in the presence of highly activated CD4 T cells. These data indicated that the ehrlichiae maintain chronic infection not by inhibiting antigen presentation or T-cell activation but, in part, by avoiding signals mediated by activated T cells.
主要组织相容性复合体/肽抗原呈递给CD4 T细胞的时空变化如何在细胞内细菌感染期间调节CD4 T细胞反应,这方面相对未被探索。我们已经表明,用埃立克体的外膜蛋白OMP-19免疫可保护小鼠免受致命的埃立克体攻击感染,并且我们鉴定出一个CD4 T细胞表位(IA(b)/OMP-19(107-122)),在免疫或感染后可引发CD4 T细胞。在此,我们使用IA(b)/OMP-19(107-122)特异性T细胞系来监测在感染小鼠埃立克体(一种在C57BL/6小鼠中建立持续感染的细菌)的急性和慢性感染期间的体外抗原呈递。通过测量T细胞系细胞内γ干扰素(IFN-γ)的产生来检测宿主抗原呈递细胞对IA(b)/OMP-19(107-122)的呈递。静脉感染后,在脾脏、腹腔渗出细胞和淋巴结中检测到抗原呈递,尽管不同组织中抗原呈递的动力学有所不同。在每个解剖部位,抗原呈递与细菌定植密切相关,并且抗原呈递与CD4 T细胞效应功能之间存在直接关系。脾脏和淋巴结树突状细胞(DCs)是IA(b)/OMP-19(107-122)的有效呈递者,表明DCs在埃立克体感染和免疫中起重要作用。即使在存在高度活化的CD4 T细胞的情况下,慢性感染和抗原呈递也发生在腹腔内。这些数据表明,埃立克体维持慢性感染不是通过抑制抗原呈递或T细胞活化,而是部分地通过避免由活化T细胞介导的信号。