| First Author | Mai W | Year | 2019 |
| Journal | Neurol Sci | Volume | 40 |
| Issue | 4 | Pages | 779-791 |
| PubMed ID | 30671738 | Mgi Jnum | J:295539 |
| Mgi Id | MGI:6453938 | Doi | 10.1007/s10072-019-3721-2 |
| Citation | Mai W, et al. (2019) Protective effects of CX3CR1 on autoimmune inflammation in a chronic EAE model for MS through modulation of antigen-presenting cell-related molecular MHC-II and its regulators. Neurol Sci 40(4):779-791 |
| abstractText | BACKGROUND: Recent evidences have implicated neuroprotective effects of CX3CR1 in multiple sclerosis (MS). But whether CX3CR1 is involved in modulation of antigen-presenting cell (APC)-related molecular MHC-II and what the possible mechanism is remain unidentified. OBJECTIVE: In this study, we intended to investigate the effects of CX3CR1 on MHC-II expressions on brain myeloid cells in experimental autoimmune encephalomyelitis (EAE) mice and explore the possible regulators for it. METHODS: CX3CR1-deficient EAE mice were created. Disease severity, pathological damage, and the expressions of MHC-II and its mediators on myeloid cells were detected. RESULTS: We found that compare with wile-typed EAE mice, CX3CR1-deficient EAE mice exhibited more severe disease severity. An accumulation of CD45(+)CD115(+)Ly6C(-)CD11c(+) cells was reserved in the affected EAE brain of CX3CR1-deficient mice, consistent with disease severity and pathological damage in the brain. The expressions of MHC-II on the brain CD45(+)CD115(+)Ly6C(-)CD11c(+) cells of CX3CR1-deficient EAE mice were elevated, in accord with the increased protein and mRNA expressions of class II transactivator (CIITA) and interferon regulatory factor-1 (IRF-1). CONCLUSIONS: The findings indicated that CX3CR1 might be an important regulator for MHC-II expressions on APCs, playing a beneficial role in EAE. The mechanism was probably through regulation on the MHC-II regulators CIITA and IRF-1. |
