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Updated: May 10, 2026
Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis
Published on: December 1, 2023
MicroRNA-132 suppresses autoimmune encephalomyelitis by inducing cholinergic anti-inflammation: a new Ahr-based
Hamza Hanieh1, Abdullah Alzahrani
1Biological Sciences Department, King Faisal University, Ahsaa, Saudi Arabia.
Abstract:
MicroRNAs (miRNAs) are a small group of RNAs that are emerging as a new avenue by which autoimmune diseases may be modulated. Accumulating evidence shows that miRNAs are involved in the pathogenesis of MS; however, the interaction of miRNAs with environmentally responsive transcription factors that play prominent roles in MS is unexplored. The activation of aryl hydrocarbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alleviates inflammation in experimental autoimmune encephalomyelitis (EAE), the best available model of MS. Therefore, we predicted that TCDD could attenuate EAE by inducing miRNA(s) targeting inflammatory mediators. Here, we show that TCDD induces cholinergic anti-inflammation in EAE mice by upregulating acetylcholinesterase-targeting miR-132. The expression of miR-132 was downregulated in CD4⁺ cells and associated with EAE severity, while TCDD treatment attenuated EAE by inducing the miR-132/acetylcholinesterase module. Silencing miR-132 in vivo abolished TCDD-induced cholinergic anti-inflammation and aggravated EAE. Overexpression of miR-132 in encephalitogenic CD4⁺ cells decreased IL-17 and IFN-γ and suppressed T-cell proliferation. In conclusion, our findings identify a new miRNA-based mechanism through which miR-132 mediates TCDD-induced EAE attenuation, suggesting that miR-132 could be a promising therapeutic target for anti-inflammatory treatment of MS.
Insights
MicroRNAs (miRNAs) like miR-132 are key in multiple sclerosis (MS) pathogenesis. TCDD treatment upregulates miR-132, reducing inflammation and attenuating experimental autoimmune encephalomyelitis (EAE) in mice.
Area of Science:
- Immunology
- Neuroscience
- Molecular Biology
Background:
- MicroRNAs (miRNAs) are implicated in autoimmune disease pathogenesis, including multiple sclerosis (MS).
- The role of miRNAs interacting with environmental factors in MS remains largely unexplored.
- 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) activates the aryl hydrocarbon receptor, reducing inflammation in experimental autoimmune encephalomyelitis (EAE), a model for MS.
Purpose of the Study:
- To investigate the potential of TCDD in attenuating EAE by inducing specific miRNAs.
- To elucidate the role of miR-132 in TCDD-mediated anti-inflammatory effects in EAE.
- To explore miR-132 as a potential therapeutic target for MS.
Main Methods:
- TCDD administration in EAE mice.
- Quantification of miR-132 expression in CD4+ cells.
- In vivo silencing and overexpression of miR-132.
- Assessment of T-cell proliferation and cytokine production (IL-17, IFN-γ).
Main Results:
- TCDD treatment upregulated miR-132 expression in EAE mice, correlating with reduced EAE severity.
- miR-132 expression was downregulated in CD4+ cells of EAE mice.
- Silencing miR-132 abolished TCDD's anti-inflammatory effects and worsened EAE.
- Overexpressing miR-132 suppressed T-cell proliferation and reduced IL-17 and IFN-γ production.
Conclusions:
- TCDD attenuates EAE by inducing the miR-132/acetylcholinesterase pathway, demonstrating a novel miRNA-based anti-inflammatory mechanism.
- miR-132 plays a critical role in mediating TCDD's therapeutic effects in EAE.
- miR-132 represents a potential therapeutic target for developing anti-inflammatory strategies for MS.
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