MHC class II exacerbates demyelination in vivo independently of T cells

被引：65

作者：

Hiremath, Meenaxi M. ^{[2
,4
]}

Chen, Vivian S. ^{[2
,4
]}

Suzuki, Kinuko ^{[1
,2
,3
]}

Ting, Jenny P. -Y. ^{[1
,4
,5
]}

Matsushima, Glenn K. ^{[1
,2
,4
,6
]}

机构：

[1] Univ N Carolina, Curriculum Neurobiol, Chapel Hill, NC 27599 USA

[2] Univ N Carolina, UNC Neurosci Ctr, Chapel Hill, NC 27599 USA

[3] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA

[4] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA

[5] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

[6] Univ N Carolina, Program Mol Biol & Biotechnol, Chapel Hill, NC 27599 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2008年 / 203卷 / 01期

关键词：

Major histocompatibility complex class II; Microglia; T cells; Myelination; Cuprizone intoxication model;

D O I：

10.1016/j.jneuroim.2008.06.034

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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-A(beta)(-/-) 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-1 beta, TNF-alpha, 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. (C) 2008 Elsevier B.V. All rights reserved.

引用

页码：23 / 32

页数：10

共 99 条

[91] ALTERED I-A PROTEIN-MEDIATED TRANSMEMBRANE SIGNALING IN B-CELLS THAT EXPRESS TRUNCATED I-AK PROTEIN [J].