ArticleJournal of immunology (Baltimore, Md. : 1950)2009
NKG2A inhibits invariant NKT cell activation in hepatic injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Unconventional T cells in urological cancers: catch them if you can.Nature reviews. Urology · 2026Review
- Tumor-infiltrating lymphocytes and tumor-associated macrophages in cancer immunoediting: a targetable therapeutic axis.Frontiers in immunology · 2025Review
- Article
- Review
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- Role of NK-Like CD8Infection and immunity · 2022Article
- Human intestinal and circulating invariant natural killer T cells are cytotoxic against colorectal cancer cells via the perforin-granzyme pathway.Molecular oncology · 2021Article
- License to Kill: When iNKT Cells Are Granted the Use of Lethal Cytotoxicity.International journal of molecular sciences · 2020Review
- Personalized inherent randomness of the immune system is manifested by an individualized response to immune triggers and immunomodulatory therapies: a novel platform for designing personalized immunotherapies.Immunologic research · 2019Article
- Activation of natural killer T cells contributes to triptolide-induced liver injury in mice.Acta pharmacologica Sinica · 2018Article
- Critical Contribution of NK Group 2 Member D Expressed on Invariant Natural Killer T Cells in Concanavalin A-Induced Liver Hepatitis in Mice.Frontiers in immunology · 2018Article
- The Role of Natural Killer T Cells in Cancer-A Phenotypical and Functional Approach.Frontiers in immunology · 2018Review
- Differential pulmonic NK and NKT cell responses in Schistosoma japonicum-infected mice.Parasitology research · 2017Article
- Review
- Article
- The Inhibitory Receptor NKG2A Sustains Virus-Specific CD8⁺ T Cells in Response to a Lethal Poxvirus Infection.Immunity · 2015Article
- Transitioning from Idiopathic to Explainable Autoimmune Hepatitis.Digestive diseases and sciences · 2015Review
- Chronic alcohol consumption enhances iNKT cell maturation and activation.Toxicology and applied pharmacology · 2015Article
- Natural killer T (NKT) cells in autoimmune hepatitis.Current opinion in immunology · 2013Review
- Shared and distinct transcriptional programs underlie the hybrid nature of iNKT cells.Nature immunology · 2013Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
Abstract
Activation of invariant NKT (iNKT) cells in the liver is generally regarded as the critical step for Con A-induced hepatitis, and the role of NK cell receptors for iNKT cell activation is still controversial. In this study we show that blockade of the NKG2A-mediated inhibitory signal with antagonistic anti-NKG2A/C/E mAb (20d5) aggravated Con A-induced hepatitis in wild-type, Fas ligand (FasL)-mutant gld, and IL-4-deficient mice even with NK cell and CD8 T cell depletion, but not in perforin-, IFN-gamma-, or IFN-gamma- and perforin-deficient mice. Consistently, 20d5 pretreatment augmented serum IFN-gamma levels and perforin-dependent cytotoxicity of liver mononuclear cells following Con A injection, but not their FasL/Fas-dependent cytotoxicity. However, blockade of NKG2A-mediated signals during the cytotoxicity effector phase did not augment cytotoxic activity. Activated iNKT cells promptly disappeared after Con A injection, whereas NK1(-) iNKT cells, which preferentially expressed CD94/NKG2A, predominantly remained in the liver. Pretreatment with 20d5 appeared to facilitate disappearance of iNKT cells, particularly NK1(-) iNKT cells. Moreover, Con A-induced and alpha-galactosylceramide-induced hepatic injury was very severe in CD94/NKG2A-deficient DBA/2J mice compared with CD94/NKG2A-intact DBA/2JJcl mice. Overall, these results indicated that a NKG2A-mediated signal negatively regulates iNKT cell activation and hepatic injury.
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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.