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CXCR3 signaling in glial cells ameliorates experimental autoimmune encephalomyelitis by restraining the generation of a pro-Th17 cytokine milieu and reducing CNS-infiltrating Th17 cells
BACKGROUND: Experimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis (MS). It has been shown that Th17 cells are critical for EAE pathogenesis. Mice lacking CXCR3 develop aggravated EAE compared with wild-type (WT) mice. This study investigated the effect of CXCR3 on Th...
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| Pubblicato in: | J Neuroinflammation |
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| Autori principali: | , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
BioMed Central
2016
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4828793/ https://ncbi.nlm.nih.gov/pubmed/27068264 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/s12974-016-0536-4 |
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