ReviewJournal of molecular medicine (Berlin, Germany)2018
Antigen-presenting cell diversity for T cell reactivation in central nervous system autoimmunity.
Review in Journal of molecular medicine (Berlin, Germany), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Prohibitin 2 is a key regulator of T cell proliferation, differentiation, and effector functions in vivo.Communications biology · 2026Article
- Astrocytic but not Microglial Antigen Presentation Shapes Protective Immunity to Toxoplasma gondii in the Brain.Research square · 2026Article
- From Demyelination to Intervention: Natural Compounds as Emerging Therapeutic Targets in Multiple Sclerosis Neuroinflammation.Journal of immunology research · 2026Review
- Activation and Long-Term Maintenance of Adaptive Immunity in the Central Nervous System: A Double-Edged Sword?CNS neuroscience & therapeutics · 2025Review
- Article
- Immunomodulatory effects of HYCO-3, a dual action CO-releaser/Nrf2 activator.Clinical and experimental immunology · 2025Article
- Engineering neuroimmune regulation: biomaterial and nanotechnology platforms for neuropathology diagnosis and targeted immunomodulation.Frontiers in immunology · 2025Review
- Emerging Insights into the Role of Macrophages in Multiple Sclerosis: Pathogenesis and Potential Therapeutic Strategies.Journal of inflammation research · 2025Review
- T Cells Trafficking into the Brain in Aging and Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Single-Cell RNA Sequencing Transcriptomics Revealed HCMV IE2-Related Microglia Responses in Alzheimer's-Like Disease in Transgenic Mice.Molecular neurobiology · 2024Article
- Role of autoreactive Tc17 cells in the pathogenesis of experimental autoimmune encephalomyelitis.Neuroprotection (Chichester, England) · 2024Article
- Discrete class I molecules on brain endothelium differentially regulate neuropathology in experimental cerebral malaria.Brain : a journal of neurology · 2024Article
- A20 regulates lymphocyte adhesion in murine neuroinflammation by restricting endothelial ICOSL expression in the CNS.The Journal of clinical investigation · 2023Article
- Immune Cell Contributors to the Female Sex Bias in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis.Current topics in behavioral neurosciences · 2023Article
- Phenethyl Ester of Gallic Acid Ameliorates Experimental Autoimmune Encephalomyelitis.Molecules (Basel, Switzerland) · 2022Article
- MOG-Specific T Cells Lead to Spontaneous EAE with Multilocular B Cell Infiltration in the GF-IL23 Model.Neuromolecular medicine · 2022Article
- Multiple Receptors Involved in Invasion and Neuropathogenicity of Canine Distemper Virus: A Review.Viruses · 2022Review
- Activation pathways that drive CD4Immunological reviews · 2022Review
- EPC infusion ameliorates acute graft-versus-host disease-related endothelial injury after allogeneic bone marrow transplantation.Frontiers in immunology · 2022Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Autoreactive T cells are considered the major culprits in the pathogenesis of many autoimmune diseases like multiple sclerosis (MS). Upon activation in the lymphoid organs, autoreactive T cells migrate towards the central nervous system (CNS) and target the myelin sheath-forming oligodendrocytes, resulting in detrimental neurological symptoms. Despite the availability of extensively studied systems like the experimental autoimmune encephalomyelitis (EAE) model, our understanding of this disease and the underlying pathogenesis is still elusive. One vividly discussed subject represents the T cell reactivation in the CNS. In order to exert their effector functions in the CNS, autoreactive T cells must encounter antigen-presenting cells (APCs). This interaction provides an antigen-restricted stimulus in the context of major histocompatibility complex class II (MHC-II) and other co-stimulatory molecules. Peripherally derived dendritic cells (DCs), B cells, border-associated macrophages (BAM), CNS-resident microglia, and astrocytes have the capacity to express molecules required for antigen presentation under inflammatory conditions. Also, endothelial cells can fulfill these prerequisites in certain situations. Which of these cells in fact act as APCs for T cell reactivation and to which extent they can exert this function has been studied intensively, but unfortunately with no firm conclusion. In this review, we will summarize the findings that support or question the antigen presenting capacities of the mentioned cell types of CNS-localized T cell reactivation.
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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.