ArticleFrontiers in neurology2020
Rapamycin Alleviates the Symptoms of Multiple Sclerosis in Experimental Autoimmune Encephalomyelitis (EAE) Through Mediating the TAM-TLRs-SOCS Pathway.
Article in Frontiers in neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The dual role of mTOR in multiple sclerosis pathophysiology: a systematic review.Journal of neurology · 2026Pooled it
- Immunometabolic reprogramming in multiple sclerosis: from pathogenic amplifier to therapeutic target in neuroinflammation and remyelination.Inflammopharmacology · 2026Review
- MOG-Peptide Synergizes With Rapamycin to Drive CD4Immunology · 2026Article
- Decoding the PI3K/Akt/mTOR-JAK/STAT signaling axis in multiple sclerosis: mechanistic crosstalk and therapeutic opportunities.Immunologic research · 2026Review
- Regulation and Interaction Among SOCS1 and SOCS3 by MicroRNAs in Multiple Sclerosis: A Review andThe Yale journal of biology and medicine · 2026Review
- Glial Cytokine and Metabolic Networks in Progressive Multiple Sclerosis: From Pathophysiology to Biomarkers and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Interaction between Th17 and central nervous system in multiple sclerosis.Brain, behavior, & immunity - health · 2025Review
- Research progress of SOCS in autoimmune diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- IRF5 mediates adaptive immunity via altered glutamine metabolism, mTORC1 signaling and post-transcriptional regulation following T cell receptor activation.bioRxiv : the preprint server for biology · 2024Article
- Article
- Neuroprotective effect of curcumin against experimental autoimmune encephalomyelitis-induced cognitive and physical impairments in mice: an insight into the role of the AMPK/SIRT1 pathway.Inflammopharmacology · 2024Article
- Administration methods and dosage of poly(lactic acid)-glycol intervention to myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalitis mice.BMC neuroscience · 2024Article
- A Stable Micellar Formulation of RAD001 for Intracerebroventricular Delivery and the Treatment of Alzheimer's Disease and Other Neurological Disorders.International journal of molecular sciences · 2023Article
- Article
- The role of secreted proteins in efferocytosis.Frontiers in cell and developmental biology · 2023Review
- Enhancing the functionality of self-assembled immune signals using chemical crosslinks.Frontiers in immunology · 2023Article
- IL-34 deficiency impairs FOXP3Clinical and translational medicine · 2022Article
- The mTOR Signaling Pathway in Multiple Sclerosis; from Animal Models to Human Data.International journal of molecular sciences · 2022Review
- AMPK-autophagy-mediated inhibition of microRNA-30a-5p alleviates morphine tolerance via SOCS3-dependent neuroinflammation suppression.Journal of neuroinflammation · 2022Article
- Analysis of shared underlying mechanism in neurodegenerative disease.Frontiers in aging neuroscience · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). Our research aimed to find an immunomodulatory therapy for MS. An experimental autoimmune encephalomyelitis (EAE) mouse model of MS was established induced with the syntheticmyelin oligodendrocyte glycoprotein peptide 35-55 (MOG35-55). Fifty C57BL/6 mice were randomly divided into the Normal group, EAE group, and Rapamycin group (EAE mice treated with three different doses of rapamycin). Hematoxylin and eosin staining and Weil myelin staining were performed on the brain tissues of mice after 21 days post-immunization. The protein expression of Gas6, Tyro3, Axl, Mer in paraventricular tissues were analyzed by immunohistochemistry. The mRNA and protein expression of Gas6, Tyro3, Axl, Mer, SOCS1, SOCS3, Toll-like receptor (TLR) 3, and TLR4 were detected by quantitative real-time PCR (qRT-PCR) and Western blot, respectively. An enzyme-linked immunosorbent assay (ELISA) was used to detect the secretion of the inflammatory factors IFN-γ and IL-17. Rapamycin treatment could ameliorate the behavior impairment in EAE mice induced by MOG35-55. The expression of Gas6, Tyro3, Axl, Mer, SOCS1, and SOCS3 were decreased in EAE mice at 21 days post-immunization, while the expression of Gas6, Tyro3, Axl, and Mer in rapamycin group was higher than that in EAE group. It was accompanied by an increase in anti-inflammatory proteins SOCS1 and SOCS3, a decrease in the inflammatory proteins TLR-3, TLR-4 and in the amount of IFN-γ, and IL-17. Rapamycin injection relieved the nerve function of and the loss of myelin sheath in the EAE mice, mainly through mediating the TAM-TLRs-SOCS signaling pathway to regulate natural immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.