ArticleJCI insight2019
TNFR2 limits proinflammatory astrocyte functions during EAE induced by pathogenic DR2b-restricted T cells.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
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- Hematopoietic monoamine oxidase A deficiency exacerbates neuroinflammation and demyelination in female but not male mice with experimental autoimmune encephalomyelitis.Frontiers in immunology · 2026Article
- Glial cell crosstalk in Parkinson's disease: Mechanisms, implications, and therapeutic strategies.Fundamental research · 2025Review
- Single intracerebroventricular TNFR2 agonist injection impacts remyelination in the cuprizone model.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
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- RGS5 augments astrocyte activation and facilitates neuroinflammation via TNF signaling.Journal of neuroinflammation · 2023Article
- Neuro-Vulnerability in Energy Metabolism Regulation: A Comprehensive Narrative Review.Nutrients · 2023Review
- Glial Cultures Differentiated from iPSCs of Patients withInternational journal of molecular sciences · 2023Article
- The Translatability of Multiple Sclerosis Animal Models for Biomarkers Discovery and Their Clinical Use.International journal of molecular sciences · 2022Review
- Glucan particles as a novel adjuvant for the induction of experimental autoimmune encephalomyelitis.Cellular immunology · 2021Article
- Neuron-specific activation of necroptosis signaling in multiple sclerosis cortical grey matter.Acta neuropathologica · 2021Article
- Astrocyte-Derived Pleiotrophin Mitigates Late-Stage Autoimmune CNS Inflammation.Frontiers in immunology · 2021Article
- Full-Length Transcriptome Sequencing: An Insight Into the Dog Model of Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Review
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune neuroinflammatory disease where the underlying mechanisms driving disease progression have remained unresolved. HLA-DR2b (DRB1*15:01) is the most common genetic risk factor for MS. Additionally, TNF and its receptors TNFR1 and TNFR2 play key roles in MS and its preclinical animal model, experimental autoimmune encephalomyelitis (EAE). TNFR2 is believed to ameliorate CNS pathology by promoting remyelination and Treg function. Here, we show that transgenic mice expressing the human MHC class II (MHC-II) allele HLA-DR2b and lacking mouse MHC-II and TNFR2 molecules, herein called DR2bΔR2, developed progressive EAE, while disease was not progressive in DR2b littermates. Mechanistically, expression of the HLA-DR2b favored Th17 cell development, whereas T cell-independent TNFR2 expression was critical for restraining of an astrogliosis-induced proinflammatory milieu and Th17 cell responses, while promoting remyelination. Our data suggest the TNFR2 signaling pathway as a potentially novel mechanism for curtailing astrogliosis and promoting remyelination, thus providing new insights into mechanisms limiting progressive MS.
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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.