ArticleFrontiers in immunology2019
NKG2D and Its Ligand MULT1 Contribute to Disease Progression in a Mouse Model of Multiple Sclerosis.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- The Metabolic Regulation of the NKG2D-Positive NK and T Cells and Their Role in Disease Progression.Biomolecules · 2025Review
- The role of selected NKG2DLs such as MICA, MICB and ULBP4 as potential markers in multiple sclerosis.Scientific reports · 2025Article
- Role of innate immune cells in multiple sclerosis.Frontiers in immunology · 2025Review
- Bystander activated CD8Nature communications · 2024Article
- The current state of knowledge on the role of NKG2D ligands in multiple sclerosis and other autoimmune diseases.Frontiers in molecular neuroscience · 2024Review
- The Role of NKG2D and Its Ligands in Autoimmune Diseases: New Targets for Immunotherapy.International journal of molecular sciences · 2023Review
- Impact of NKG2D Signaling on Natural Killer and T-Cell Function in Cerebral Ischemia.Journal of the American Heart Association · 2023Article
- Stress Signal ULBP4, an NKG2D Ligand, Is Upregulated in Multiple Sclerosis and Shapes CD8Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- Alterations of peripheral nerve excitability in an experimental autoimmune encephalomyelitis mouse model for multiple sclerosis.Journal of neuroinflammation · 2020Article
- NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells.The Journal of experimental medicine · 2020Article
- Kupffer Cells Regulate Natural Killer Cells Via the NK group 2, Member D (NKG2D)/Retinoic Acid Early Inducible-1 (RAE-1) Interaction and Cytokines in a Primary Biliary Cholangitis Mouse Model.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NKG2D is an activating receptor expressed on the surface of immune cells including subsets of T lymphocytes. NKG2D binds multiple ligands (NKG2DL) whose expression are differentially triggered in a cell type and stress specific manner. The NKG2D-NKG2DL interaction has been involved in autoimmune disorders but its role in animal models of multiple sclerosis (MS) remains incompletely resolved. Here we show that NKG2D and its ligand MULT1 contribute to the pathobiology of experimental autoimmune encephalomyelitis (EAE). MULT1 protein levels are increased in the central nervous system (CNS) at EAE disease peak; soluble MULT1 is elevated in the cerebrospinal fluid of both active and passive EAE. We establish that such soluble MULT1 enhances effector functions (e.g., IFNγ production) of activated CD8 T lymphocytes from wild type but not from NKG2D-deficient (
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