Jones-Carson Jessica, McCollister Bruce D, Clambey Eric T, Vázquez-Torres Andrés
Department of Microbiology, UCHSC School of Medicine at Fitzsimons, University of Colorado Health Sciences Center, Aurora, CO 80010, USA.
Infect Immun. 2007 Jun;75(6):2708-16. doi: 10.1128/IAI.01905-06. Epub 2007 Apr 2.
To better understand the evolution of a systemic memory response to a mucosal pathogen, we monitored antigen-specific OT1 CD8 T-cell responses to a fusion of the SspH2 protein and the peptide SIINFEKL stably expressed from the chromosome of Salmonella enterica and loaded into the class I pathway of antigen presentation of professional phagocytes through the Salmonella pathogenicity island 2 type III secretion system (TTSS). This strategy has revealed that effector memory CD8 T cells with low levels of CD62L expression (CD62L(low)) are maintained in systemic sites months after vaccination in response to low-grade infections with Salmonella. However, the CD8 T-cell pool eventually declines. Low numbers of central memory cells surviving after prolonged resting from an antigen encounter can nevertheless reconstitute the systemic effector memory pool in a route-specific recall response to cognate antigens encountered in the gut. Accordingly, populations of CD62L(high) interleukin-7 receptor-positive progenitor central memory cells grafted into naïve mice expand in response to orally administered Salmonella expressing the chromosomal translational fusion of sspH2 and the sequence encoding the SIINFEKL peptide but fail to proliferate following systemic stimulation. Moreover, populations of systemic memory CD8 T cells restricted to Salmonella in oral vaccines selectively expand in response to cognate antigens presented by cells isolated from mesenteric lymph nodes (MLN). Together, these findings have revealed the imprinting of systemic CD8 central memory T-cell recall responses against enteropathogens by MLN. MLN restriction represents a novel mechanism by which systemic CD8 T-cell immunity is confined to periods of high risk for extraintestinal dissemination.
为了更好地理解对黏膜病原体的系统性记忆反应的演变,我们监测了抗原特异性OT1 CD8 T细胞对SspH2蛋白与肽SIINFEKL融合体的反应,该融合体由肠炎沙门氏菌染色体稳定表达,并通过沙门氏菌致病岛2型III分泌系统(TTSS)加载到专职吞噬细胞的I类抗原呈递途径中。这一策略揭示,在接种疫苗数月后,低水平表达CD62L(CD62L(low))的效应记忆CD8 T细胞因对沙门氏菌的轻度感染而维持在全身部位。然而,CD8 T细胞库最终会减少。尽管在长时间未接触抗原后处于静止状态仍存活的少量中枢记忆细胞,能够在对肠道中遇到的同源抗原的途径特异性回忆反应中重建全身效应记忆库。因此,移植到未接触过抗原的小鼠体内的CD62L(high)白细胞介素-7受体阳性祖细胞中枢记忆细胞群体,会在口服表达sspH2与编码SIINFEKL肽序列的染色体翻译融合体的沙门氏菌后发生扩增,但在全身刺激后无法增殖。此外,口服疫苗中局限于沙门氏菌的全身记忆CD8 T细胞群体,会在对从肠系膜淋巴结(MLN)分离的细胞呈递的同源抗原的反应中选择性扩增。这些发现共同揭示了MLN对针对肠道病原体的全身CD8中枢记忆T细胞回忆反应的印记作用。MLN限制代表了一种新机制,通过该机制全身CD8 T细胞免疫被限制在肠外播散高风险期。