Failure to induce experimental allergic encephalitis in mice lucking expression of SLC chemokine.

实验性过敏性脑炎（EAE）是人类多发性硬化的小鼠模型。淋巴结T细胞（plt）缺乏SLC （CCL21）和ELC （CCL19）趋化因子的表达。MOG肽免疫在对照小鼠中可诱导实验性变应性脑炎，而在plt小鼠中无诱导作用。将经MOG肽免疫的+/plt-C56BL/6小鼠体内的T细胞转移到plt小鼠体内，可发生EAE，提示plt小鼠发生EAE的失败不是由于趋化因子表达不足导致的迁移失败，而是由于效应T细胞发育所致。小鼠缺乏SLC和ELC趋化因子的表达，但T细胞对蛋白抗原皮下免疫的反应高于对照组，且持续时间远长于对照组。这些发现表明，移植小鼠的T细胞免疫调节不足。与对照小鼠相比，plt小鼠引流淋巴模式的凋亡明显减少，这导致应答T细胞数量增加。为了阐明小鼠EAE发生失败的机制，我们将分析蛋白抗原免疫后的效应CD4+ T细胞

Experimental allergic encephalitis (EAE) is a mouse model of human multiplesclerosis. Paucity of lymph node T cells (plt) mouse lacks expression of SLC (CCL21) and ELC (CCL19) chemokines. Immunization with MOG peptide induces experimental allergic encephalitis in control mice, but not in plt mice. When T cells were transferred from +/plt-C56BL/6mice immunized with MOG peptide into pltmice, EAE was deloped, suggesting that failure to develop EAE in pltmice was not due to migration failure induced by lacking chemokine expression, but due to effector T cell developmentpltmice lack expression of SLC and ELC chemokines, but T cell response to subcutaneous immunization with a protein antigen was rather higher than in control mice and prolonged much longer than in control mice. These findings suggest that T cell immune regulation is insufficient in pltmice. Apoptosis in draining lymph mode in pltmice was much less evident in pltmice than in control mice, which resulted in keeping increased number of responding T cells. To elucidate the mechanisms for the failure to develop EAE in pltmice, we will analyze effector CD4+ T cells after immunization with protein antigen