Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3065130 | Journal of Neuroimmunology | 2008 | 10 Pages |
Abstract
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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Authors
Meenaxi M. Hiremath, Vivian S. Chen, Kinuko Suzuki, Jenny P.-Y. Ting, Glenn K. Matsushima,