Weihua Mai1, Xingwei Liu2, Junfeng Wang3, Jing Zheng4, Xiao Wang2, Wenying Zhou5. 1. Department of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, NO. 52 East Meihua Road, Zhuhai, 519000, Guangdong Province, China. weihuamai2004@163.com. 2. Department of General Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China. 3. Department of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, NO. 52 East Meihua Road, Zhuhai, 519000, Guangdong Province, China. 4. Department of Nephrology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China. 5. Department of Laboratory Science, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Abstract
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.
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.
Entities:
Keywords:
CX3CR1; Class II transactivator; Experimental autoimmune encephalomyelitis; Interferon regulatory factor-1; Major histocompatibility complex class II molecules; Multiple sclerosis
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