MHC class II exacerbates demyelination in vivo independently of T cells.

MHC class II exacerbates demyelination in vivo independently of T cells.
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DOI:
10.1016/j.jneuroim.2008.06.034
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发表时间:
2008-10-15
影响因子:
3.3
通讯作者:
Matsushima GK
Matsushima GK
中科院分区:
医学4区
文献类型:
--
作者:
Hiremath MM;Chen VS;Suzuki K;Ting JP;Matsushima GK

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We have shown previously the importance of MHC class II for central nervous system remyelination; however, the function of MHC class II during cuprizone-induced demyelination has not been examined. Here, we show that I-Aβ−/− mice exhibit significantly reduced inflammation and demyelination. RAG-1−/− mice are indistinguishable from controls, indicating T cells may not play a role. The role of MHC class II depends on an intact cytoplasmic tail that leads to the production of IL-1β, TNF-α, and nitric oxide, and oligodendrocyte apoptosis. Thus, the function of MHC class II cytoplasmic tail appears to increase microglial proliferation and activation that exacerbates demyelination.
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