ArticleThe Journal of experimental medicine2020
NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Correlations between major depressive disorder, splenic morphology, and immune function.BMC psychiatry · 2025Trial
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- Targeting NK cell CLEC12B enhances cancer immunotherapy.Nature immunology · 2026Article
- A pathogenic CD4 T cell phenotype in experimental uveitis shares common features with other immune mediated inflammatory diseases.Discovery immunology · 2026Article
- Regulatory roles of 13 types of RNA modifications in osteoarthritis: based on bulk and single-cell RNA analysis.3 Biotech · 2025Article
- From genetic variants to therapeutic targets: insights into understanding rheumatoid arthritis.Frontiers in immunology · 2025Review
- Targeting the chromatin structural changes of antitumor immunity.Journal of pharmaceutical analysis · 2024Review
- Th17 Cell and Inflammatory Infiltrate Interactions in Cutaneous Leishmaniasis: Unraveling Immunopathogenic Mechanisms.Immune network · 2024Review
- NKG2D-mediated detection of metabolically stressed hepatocytes by innate-like T cells is essential for initiation of NASH and fibrosis.Science immunology · 2023Article
- Vector-based SARS-CoV-2 vaccination is associated with improved T-cell responses in hematological neoplasia.Blood advances · 2023Article
- Cytokinopathy with aberrant cytotoxic lymphocytes and profibrotic myeloid response in SARS-CoV-2 mRNA vaccine-associated myocarditis.Science immunology · 2023Article
- DisseminatedOpen forum infectious diseases · 2023Article
- Inhibition of hepatic natural killer cell function via the TIGIT receptor in schistosomiasis-induced liver fibrosis.PLoS pathogens · 2023Article
- Metabolic Reprogramming of NK Cells by Black Phosphorus Quantum Dots Potentiates Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- IL-17a-producing γδT cells and NKG2D signaling mediate bacterial endotoxin-induced neonatal lung injury: implications for bronchopulmonary dysplasia.Frontiers in immunology · 2023Article
- The immune role of the intestinal microbiome in knee osteoarthritis: a review of the possible mechanisms and therapies.Frontiers in immunology · 2023Review
- [Role of innate receptors in chronic inflammation and autoimmunity].Zeitschrift fur Rheumatologie · 2022Review
- Age as a risk factor in vasculitis.Seminars in immunopathology · 2022Review
- Stress Signal ULBP4, an NKG2D Ligand, Is Upregulated in Multiple Sclerosis and Shapes CD8Neurology(R) neuroimmunology & neuroinflammation · 2022Article
- NKG2D signaling regulates IL-17A-producing γδT cells in mice to promote cancer progression.Discovery immunology · 2022Article
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 6 countries.
Funding
Abstract
NKG2D is a danger sensor expressed on different subsets of innate and adaptive lymphocytes. Despite its established role as a potent activator of the immune system, NKG2D-driven regulation of CD4+ T helper (Th) cell-mediated immunity remains unclear. In this study, we demonstrate that NKG2D modulates Th1 and proinflammatory T-bet+ Th17 cell effector functions in vitro and in vivo. In particular, NKG2D promotes higher production of proinflammatory cytokines by Th1 and T-bet+ Th17 cells and reinforces their transcription of type 1 signature genes, including Tbx21. Conditional deletion of NKG2D in T cells impairs the ability of antigen-specific CD4+ T cells to promote inflammation in vivo during antigen-induced arthritis and experimental autoimmune encephalomyelitis, indicating that NKG2D is an important target for the amelioration of Th1- and Th17-mediated chronic inflammatory diseases.
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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.