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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Lack of ICAM-1 on APCs during T Cell Priming Leads to Poor Generation of Central Memory Cells.
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Lack of ICAM-1 on APCs during T Cell Priming Leads to Poor Generation of Central Memory Cells.

机译：在T细胞启动期间，APC上缺乏ICAM-1导致中央记忆细胞生成不良。

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摘要

ICAM-1/LFA-1 interactions are known to enhance T cell/APC interactions and to promote T cell activation and cytokine secretion. We have analyzed the consequences of ICAM-1-mediated signaling on the generation of memory T cell subsets. We report that lack of ICAM-1 on APCs, but not on T cells, leads to poor T cell activation and proliferation in vitro and in vivo, and that the defect can be compensated by Ag dose, exogenous IL-2, additional costimulation, and by increasing responder T cell density on APCs. ICAM-1-null mice do not respond to immunization with OVA peptide, but immunization with OVA or with Salmonella typhimurium leads to good T cell proliferation 7-10 days later, and clearance of a challenge infection is equivalent to that of wild-type mice. However, when followed over time, recall proliferation and antibacterial immunity decay rapidly in ICAM-1-null mice, while recall cytokine responses are unaffected. The decline in immunity is not related to poor survival of T cells activated on ICAM-1-null APCs, or to poor generation of effectors in ICAM-1-null mice. Phenotypic analysis of T cells stimulated on ICAM-1-null APCs reveals preferential generation of CD44(high)CD62L(low) effector memory cells (T(EM)) over CD44(high)CD62L(high) central memory cells (T(CM)). Further, while the proportion of naive:memory T cells is similar in unmanipulated wild-type and ICAM-1-null mice, there is an accumulation of T(EM) cells, and a high T(EM): T(CM) ratio in aging ICAM-1-null mice. Together, the data indicate that signaling through LFA-1 during T cell activation may be involved in commitment to a proliferation-competent memory pool.
机译：已知ICAM-1 / LFA-1相互作用可增强T细胞/ APC相互作用并促进T细胞活化和细胞因子分泌。我们已经分析了ICAM-1介导的信号传导对记忆T细胞亚群产生的影响。我们报告说，缺乏APC而不是T细胞的ICAM-1，会导致T细胞在体外和体内的活化和增殖不良，并且该缺陷可以通过Ag剂量，外源IL-2，其他共刺激来补偿，并通过增加APC上的响应T细胞密度来实现。 ICAM-1无效的小鼠对OVA肽的免疫反应无反应，但用OVA或鼠伤寒沙门氏菌免疫可在7-10天后产生良好的T细胞增殖，攻击性感染的清除率与野生型小鼠相同。但是，随时间推移，召回增殖和抗菌免疫力在ICAM-1无效的小鼠中迅速衰减，而召回的细胞因子反应却不受影响。免疫力的下降与在ICAM-1-null APC上激活的T细胞存活不良或在ICAM-1-null小鼠中效应子的产生不相关。对在ICAM-1空APC上刺激的T细胞的表型分析显示，相对于CD44（高）CD62L（高）中央记忆细胞（T（CM），优先产生CD44（高）CD62L（低）效应记忆细胞（T（EM）） ））。此外，尽管未操纵的野生型小鼠和ICAM-1无效小鼠中的幼稚：记忆T细胞的比例相似，但存在T（EM）细胞积聚，并且T（EM）：T（CM）比率高在衰老的ICAM-1无小鼠中。总之，这些数据表明在T细胞活化过程中通过LFA-1进行信号传导可能参与了对具有增殖能力的记忆库的承诺。

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