Altered neuroantigen-specific cytokine secretion in a Th2 environment reduces experimental autoimmune encephalomyelitis
Altered neuroantigen-specific cytokine secretion in a Th2 environment reduces experimental autoimmune encephalomyelitis
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DOI：
10.1016/j.jneuroim.2006.05.015
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发表时间：
2006-09-01
影响因子：
3.3
通讯作者：
Stohlman, Stephen A.
中科院分区：
文献类型：
--
作者：
Kirwin, Stefanie J.;Dowdell, Kenichi C.;Stohlman, Stephen A.
Th2细胞的激活抑制了临床实验性自身免疫性脑炎(EAE)、脱髓鞘和Th1介导的炎症相关基因的表达。尽管中枢神经系统炎症减轻，干扰素-γ诱导小胶质细胞表达MHC-11，但Th2保护的小鼠中枢神经系统浸润物的成分与EAE小鼠相似。用流式细胞仪分析CNS浸润细胞表明，保护与减少CD4(+)T细胞募集、优先招募供者Th2细胞或增加CD25(+)CD4(+)T细胞的频率无关。相比之下，保护与神经抗原特异性Th2细胞渗入中枢神经系统的频率增加相关。这些数据表明，外周Th2细胞因子环境既影响潜在的抗原提呈细胞，也影响神经抗原特异性Th2 CD4(+)T细胞的招募和/或保留。(C)2006爱思唯尔B.V.保留所有权利。
Activation of Th2 cells suppresses clinical experimental autoimmune encephalitis (EAE), demyelination and expression of genes associated with Th1-mediated inflammation. Despite both reduced central nervous system inflammation and IFN-gamma induced MHC class 11 expression by microglia, the composition of CNS infiltrates in Th2-protected mice were similar to mice with EAE. Analysis of the CNS infiltrating cells by flow cytometry suggests that protection did not correlate with abrogation of CD4(+) T cell recruitment, preferential recruitment of donor Th2 cells or an increased frequency of CD25(+) CD4(+) T cells. By contrast, protection correlated with an increased frequency of neuroantigen-specific Th2 cells infiltrating the CNS. These data suggest that a peripheral Th2 cytokine environment influences both potential antigen presenting cells as well as recruitment and/or retention of neuroAg-specific Th2 CD4(+) T cells. (c) 2006 Elsevier B.V. All rights reserved.