Related Experiment Video
Updated: May 16, 2026

Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
Methadone diminishes neuroinflammation and disease severity in EAE through modulating T cell function
Laya Kafami1, Ifa Etesami, Mina Felfeli
1Pathobiology Department, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran; Shefa Neuroscience Research Center, Tehran, Iran. kafami@sina.tums.ac.ir
Abstract:
Methadone is known to exert modulatory effects on the immune system. We investigated the potential effects of methadone on infiltration of inflammatory cells into the spinal cord, as well as the proliferative and cytokine responses of T cells in MOG(35-55)-induced experimental autoimmune encephalomyelitis in mice. Methadone significantly suppressed clinical signs of the disease and level of inflammatory cytokines (p<0.05) produced by T cells. Moreover, invasion of inflammatory cells into the spinal cord was significantly decreased by methadone (p<0.05). Our data point to therapeutic effects of methadone and highlight the beneficial role of opioid receptor signaling in the context of autoimmune neuroinflammation.
Insights
Methadone treatment reduced disease severity and inflammatory cell infiltration in the spinal cord of mice with experimental autoimmune encephalomyelitis. This suggests a beneficial role for opioid receptor signaling in autoimmune neuroinflammation.
Area of Science:
- Neuroimmunology
- Immunology
- Pharmacology
Background:
- Methadone is known to modulate immune system responses.
- Opioid receptor signaling plays a role in neuroinflammation.
- Experimental autoimmune encephalomyelitis (EAE) is a mouse model for multiple sclerosis.
Purpose of the Study:
- To investigate the effects of methadone on T cell responses and inflammatory cell infiltration in the spinal cord.
- To explore the therapeutic potential of methadone in autoimmune neuroinflammation.
Main Methods:
- Induction of experimental autoimmune encephalomyelitis (EAE) in mice using MOG(35-55) peptide.
- Administration of methadone to EAE mice.
- Assessment of clinical signs of EAE.
- Quantification of inflammatory cell infiltration in the spinal cord.
- Evaluation of T cell proliferation and cytokine production.
Main Results:
- Methadone significantly suppressed clinical signs of EAE.
- Methadone treatment led to a significant reduction in inflammatory cytokine levels produced by T cells.
- Invasion of inflammatory cells into the spinal cord was significantly decreased in methadone-treated mice.
- p<0.05 for all significant findings.
Conclusions:
- Methadone exhibits therapeutic effects in a mouse model of autoimmune neuroinflammation.
- Opioid receptor signaling may be beneficial in managing autoimmune neuroinflammatory conditions.
- Methadone's immunomodulatory properties warrant further investigation for autoimmune diseases affecting the central nervous system.
Related Concept Videos
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Analgesia and Pain Management
