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Updated: Feb 16, 2026
Induction and Diverse Assessment Indicators of Experimental Autoimmune Encephalomyelitis
Published on: September 9, 2022
miR-23b Suppresses Leukocyte Migration and Pathogenesis of Experimental Autoimmune Encephalomyelitis by Targeting
Yuan Zhang1, Juan-Juan Han2, Xiao-Yan Liang2
1Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China; Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Abstract:
MicroRNAs (miRNAs) are small, non-coding RNAs involved in immune response regulation. Specific miRNAs have been linked to the development of various autoimmune diseases; however, their contribution to the modulation of CNS-directed cellular infiltration remains unclear. In this study, we found that miR-23b, in addition to its reported functions in the suppression of IL-17-associated autoimmune inflammation, halted the progression of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by directly inhibiting the migration of pathogenic leukocytes to the CNS. We demonstrated that miR-23b was specifically decreased during the acute phase of EAE and that overexpression of miR-23b resulted in a defect in leukocyte migration and strong resistance to EAE. Furthermore, we found that miR-23b suppressed leukocyte migration of EAE by targeting CCL7, a chemokine that attracts monocytes during inflammation and metastasis. Finally, in the adoptive transfer model, miR-23b reduced the severity of EAE by inhibiting the migration of pathogenic T cells to the CNS rather than diminishing the encephalitogenesis of T cells. Taken together, our results characterize a novel aspect of miR-23b function in leukocyte migration, and they identify miR-23b as a potential therapeutic target in the amelioration of MS and likely other autoimmune diseases.
Insights
MicroRNAs (miRNAs) regulate immune responses. This study shows miR-23b inhibits leukocyte migration to the central nervous system (CNS), halting experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS).
Area of Science:
- Immunology
- Neuroscience
- Molecular Biology
Background:
- MicroRNAs (miRNAs) are key regulators of immune responses.
- Specific miRNAs are implicated in autoimmune diseases, but their role in CNS inflammation is unclear.
- Experimental autoimmune encephalomyelitis (EAE) serves as a model for multiple sclerosis (MS).
Purpose of the Study:
- To investigate the role of miR-23b in the modulation of CNS-directed cellular infiltration in autoimmune diseases.
- To determine if miR-23b affects the progression of EAE.
- To identify the molecular mechanisms by which miR-23b influences leukocyte migration.
Main Methods:
- Assessing miR-23b levels during EAE.
- Overexpressing miR-23b in EAE models.
- Analyzing leukocyte migration and T cell responses.
- Identifying miR-23b targets using molecular assays.
- Utilizing adoptive transfer models to evaluate EAE severity.
Main Results:
- miR-23b levels were decreased during the acute phase of EAE.
- Overexpression of miR-23b inhibited leukocyte migration to the CNS and conferred resistance to EAE.
- miR-23b suppressed leukocyte migration by targeting the chemokine CCL7.
- miR-23b reduced EAE severity by inhibiting pathogenic T cell migration to the CNS.
Conclusions:
- miR-23b plays a critical role in regulating leukocyte migration into the CNS.
- miR-23b functions by targeting CCL7, thereby reducing inflammatory cell infiltration.
- miR-23b represents a potential therapeutic target for multiple sclerosis and other autoimmune diseases.
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