ArticleCell death and differentiation2022
The histone demethylase Kdm6b regulates the maturation and cytotoxicity of TCRαβ
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- JMJD3 upregulates ALOX5 to drive malignancy and concomitant ferroptosis sensitivity in gastric cancer.Cell death & disease · 2025Article
- Structural mechanism of H3K27 demethylation and crosstalk with heterochromatin markers.Molecular cell · 2025Article
- Immunoenhancing effects of Gynostemma Pentaphyllum Extract on mucosal immunity against porcine epidemic diarrhea virus.Frontiers in veterinary science · 2025Article
- NApoptosis : an international journal on programmed cell death · 2024Article
- Histone demethylases in the regulation of immunity and inflammation.Cell death discovery · 2023Review
- The role of histone methylase and demethylase in antitumor immunity: A new direction for immunotherapy.Frontiers in immunology · 2022Review
- Canine oral squamous cell carcinoma as a spontaneous, translational model for radiation and immunology research.Frontiers in oncology · 2022Article
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Authors and funding
22 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal intraepithelial lymphocytes (IELs) are distributed along the length of the intestine and are considered the frontline of immune surveillance. The precise molecular mechanisms, especially epigenetic regulation, of their development and function are poorly understood. The trimethylation of histone 3 at lysine 27 (H3K27Me3) is a kind of histone modifications and associated with gene repression. Kdm6b is an epigenetic enzyme responsible for the demethylation of H3K27Me3 and thus promotes gene expression. Here we identified Kdm6b as an important intracellular regulator of small intestinal IELs. Mice genetically deficient for Kdm6b showed greatly reduced numbers of TCRαβ
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