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Updated: Jan 30, 2026
Author Spotlight: Unveiling the Pathway Linking Obesity to Autoimmune Inflammation in Multiple Sclerosis
Published on: February 23, 2024
Protective effects of CX3CR1 on autoimmune inflammation in a chronic EAE model for MS through modulation of
Weihua Mai1, Xingwei Liu2, Junfeng Wang3
1Department of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, NO. 52 East Meihua Road, Zhuhai, 519000, Guangdong Province, China. weihuamai2004@163.com.
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.
Insights
CX3CR1 deficiency worsens experimental autoimmune encephalomyelitis (EAE) by increasing MHC-II expression on myeloid cells, likely via CIITA and IRF-1 regulators, suggesting a protective role for CX3CR1 in MS.
Area of Science:
- Neuroimmunology
- Cellular and Molecular Immunology
Background:
- CX3CR1 is implicated in neuroprotection in multiple sclerosis (MS).
- The role of CX3CR1 in modulating antigen-presenting cell (APC)-related MHC-II expression and its mechanisms in MS remains unclear.
Purpose of the Study:
- To investigate CX3CR1's effects on MHC-II expression in brain myeloid cells during experimental autoimmune encephalomyelitis (EAE).
- To explore potential regulators involved in CX3CR1-mediated MHC-II modulation in EAE.
Main Methods:
- Generated CX3CR1-deficient EAE mouse models.
- Assessed disease severity, pathological damage, and MHC-II expression on myeloid cells.
Main Results:
- CX3CR1-deficient EAE mice showed increased disease severity and pathological damage.
- Elevated MHC-II expression was observed on brain myeloid cells (CD45+CD115+Ly6C-CD11c+) in CX3CR1-deficient EAE mice.
- Increased expression of MHC-II regulators, CIITA and IRF-1, correlated with elevated MHC-II levels.
Conclusions:
- CX3CR1 plays a beneficial role in EAE by regulating MHC-II expression on APCs.
- CX3CR1 likely modulates MHC-II expression through the regulators CIITA and IRF-1.
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