Role of SLC and ELC chemokines in the development of experimental allergic encephalomyelitis as an animal model of multiple sclerosis.

实验性过敏性脑脊髓炎（EAE）是多发性硬化症的动物模型。用CFA中的髓鞘少突胶质细胞糖蛋白（MOG）35-55肽（MOG 35 - 55肽）皮下免疫C57 BL/6小鼠产生EAE。然而，C57 BL/6-plt/plt小鼠在类似处理时未发生EAE。plt小鼠存在CCL 19/CCL 21表达缺陷。因此，这些趋化因子可能参与EAE的发展。有两种可能：一是致病性T细胞向中枢神经系统的迁移失败，二是plt小鼠体内未产生致病性T细胞。为了区分这些可能性，将来自用CFA中的MOG 35 -55肽免疫的C57 BL/6野生型小鼠的T细胞静脉内转移到plt小鼠中，这导致plt小鼠中EAE的发展。当用CFA中的MOG肽静脉内免疫的这些小鼠的引流淋巴结细胞在体外用肽刺激时，来自plt小鼠的T细胞产生比来自野生型小鼠的T细胞多得多的IL-4，而IFN-γ产生相反。这些结果，虽然实验仍然是初步的，表明CCL 19/CCL 21参与了EAE诱导的致病性Th 1细胞的产生。这些趋化因子参与的机制目前正在调查中。

Experimental allergic encephalomyelitis(EAE) is an animal model for multiple sclerosis. C57BL/6 mouse immunized subcutaneously with myelin oligodendrocyte glycoprotein(MOG) 35-55 peptide(MOG35-55 peptide) in CFA developed EAE. However, C57BL/6-plt/plt mouse did not develop EAE, when similarly treated. plt mouse has a defect in the expression of CCL19/CCL21. Thus, it is possible that these chemokines are involved in the development of EAE. There were two possibilities ; one was the migration failure of pathogenic T cells into CNS, the other was that pathogenic T cells were not generated in the plt mouse. To differentiate these possibilities, T cells from C57BL/6 wild type mice immunized with MOG35-55 peptide in CFA were intravenously transferred into plt mice, which resulted in the development of EAE in plt mice. When draining lymph node cells from these mice intravenously immunized with MOG peptide in CFA, were stimulated in vitro with the peptide, T cells from plt mice produced much more IL-4 than those from wild type mice, whereas IFN-γ was inversely produced. These results, although the experiments were still preliminary, suggested that CCL19/CCL21 are involved in the generation of pathogenic Th1 cells for EAE induction. The mechanisms for the involvement of these chemokines are now under the investigation.