ReviewJournal of autoimmunity2013
Using EAE to better understand principles of immune function and autoimmune pathology.
Review in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
131 citing papers in PubMed, 2 syntheses or guidelines pooled it, 242 citations in OpenAlex.
- The Efficacy of Mesenchymal Stem Cell Therapies in Rodent Models of Multiple Sclerosis: An Updated Systematic Review and Meta-Analysis.Frontiers in immunology · 2021Pooled it
- Pooled it
- Control of naive T cell reactivity and peripheral tolerance by ascorbate and TET activity.Science advances · 2026Article
- Advancing EAE Modeling: Establishment of a Non-Pertussis Immunization Protocol for Multiple Sclerosis.Bio-protocol · 2026Article
- Stress-induced sympathetic hyperactivation drives hair follicle necrosis to trigger autoimmunity.Cell · 2026Article
- Hematopoietic monoamine oxidase A deficiency exacerbates neuroinflammation and demyelination in female but not male mice with experimental autoimmune encephalomyelitis.Frontiers in immunology · 2026Article
- The relativity of regulatory T cell suppression modes.Frontiers in immunology · 2026Review
- Oligodendrocyte progenitor cell responses to inflammatory demyelination with aging.Research square · 2025Article
- Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pidotimod alleviated experimental autoimmune encephalomyelitis by regulating the balance of splenic lymphocytes.BMC immunology · 2025Article
- Follicle on the Roof: Tertiary Lymphoid Structures in Central Nervous System Autoimmunity.Immunological reviews · 2025Review
- Article
- Target inhibition of SPAK in choroid plexus attenuates T cell infiltration and demyelination in experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2025Article
- CD4+ T cell-innate immune crosstalk is critical during Staphylococcus aureus craniotomy infection.JCI insight · 2025Article
- Obesity intensifies sex-specific interferon signaling to selectively worsen central nervous system autoimmunity in females.Cell metabolism · 2024Article
- Build muscles and protect myelin.NeuroImmune pharmacology and therapeutics · 2024Review
- Myelin-reactive B cells exacerbate CD4Nature communications · 2024Article
- Selected cannabis cultivars modulate glial activation: in vitro and in vivo studies.Journal of cannabis research · 2024Article
- The presence of Mott cells in the lymph nodes of rats with experimental autoimmune encephalomyelitis.Histochemistry and cell biology · 2024Article
- Active Induction of a Multiple Sclerosis-Like Disease in Common Laboratory Mouse Strains.Methods in molecular biology (Clifton, N.J.) · 2024Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) in which myelin becomes the target of attack by autoreactive T cells. The immune components of the disease are recapitulated in mice using the experimental autoimmune encephalomyelitis (EAE) model. EAE is classically induced by the immunization of mice with encephalitogenic antigens derived from CNS proteins such as proteolipid protein (PLP), myelin basic protein (MBP) and myelin oligodendrocyte glycoprotein (MOG). Immunization of susceptible mouse strains with these antigens will induce autoreactive inflammatory T cell infiltration of the CNS. More recently, the advent of clonal T cell receptor transgenic mice has led to the development of adoptive transfer protocols in which myelin-specific T cells may induce disease upon transfer into naïve recipient animals. When used in concert with gene knockout strains, these protocols are powerful tools by which to dissect the molecular pathways that promote inflammatory T cells responses in the central nervous system (CNS). Further, myelin-antigen-specific transgenic T cells may be cultured in vitro under a variety of conditions prior to adoptive transfer, allowing one to study the effects of soluble factors or pharmacologic compounds on T cell pathogenicity. In this review, we describe many of the existing models of EAE, and discuss the contributions that use of these models has made in understanding both T helper cell differentiation and the function of inhibitory T cell receptors. We focus on the step-by-step elucidation of the network of signals required for T helper 17 (Th17) cell differentiation, as well as the molecular dissection of the Tim-3 negative regulatory signaling pathway in Th1 cells.
Indexed as
Identifiers
What OpenQuestion holds
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.