CXCR2-positive neutrophils are essential for cuprizone-induced demyelination: relevance to multiple sclerosis.
CXCR2-positive neutrophils are essential for cuprizone-induced demyelination: relevance to multiple sclerosis.
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DOI:
10.1038/nn.2491
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发表时间:
2010-03
影响因子:
25
通讯作者:
Ransohoff, Richard M.
中科院分区:
文献类型:
--
作者:
Liu, LiPing;Belkadi, Abdelmadjid;Darnall, Lindsey;Hu, Taofang;Drescher, Caitlin;Cotleur, Anne C.;Padovani-Claudio, Dolly;He, Tao;Choi, Karen;Lane, Thomas E.;Miller, Robert H.;Ransohoff, Richard M.
Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the central nervous system (CNS). Recent studies suggest diverse mechanisms underlying demyelination, including a subset of lesions involving interplay between metabolic insult to oligodendrocytes and inflammatory mediators. For mice of susceptible strains, cuprizone feeding results in oligodendrocyte cell loss and demyelination of the corpus callosum. Remyelination ensues, and has been extensively studied. Cuprizone-induced demyelination remains incompletely characterized. Here we show that mice lacking type 2 CXC chemokine receptor (CXCR2) are relatively resistant to cuprizone-induced demyelination, and CXCR2+ neutrophils from the circulation play an essential role in cuprizone-induced demyelination. Findings support a novel two-hit process of cuprizone-induced demyelination, mirroring proposals about pathogenesis of MS lesions featuring extensive oligodendrocyte cell loss. These data indicate that cuprizone-induced demyelination will provide a useful model for certain aspects of MS pathogenesis.
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影响因子:
11.2
作者:
Fuller, Molly L.;DeChant, Anne K.;Miller, Robert H.
通讯作者:
Miller, Robert H.
DOI:
10.1093/jnen/63.3.262
发表时间:
2004-03-01
影响因子:
3.2
作者:
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通讯作者:
Ransohoff, RM
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通讯作者:
Popko, B
影响因子:
4.4
作者:
Liu, LiPing;Huang, DeRen;Ransohoff, Richard M.
通讯作者:
Ransohoff, Richard M.