ArticleJournal of immunology (Baltimore, Md. : 1950)2022
Cutting Edge: The Expression of Transcription Inhibitor GFI1 Is Induced by Retinoic Acid to Rein in Th9 Polarization.
Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- GFI1 as a novel regulator of γδ T cell development and the IL-17/IFN-γ lineage commitment.Frontiers in immunology · 2026Article
- Platelets as a potential new immune coordinator in T cell-mediated aplastic anemia.Frontiers in oncology · 2025Review
- EPRIM: An approach of identifying cancer immune-related epigenetic regulators.Molecular therapy. Nucleic acids · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
IL-9, produced mainly by specialized T cells, mast cells, and group 2 innate lymphoid cells, regulates immune responses, including anti-helminth and allergic responses. Polarization of naive CD4 T cells into IL-9-producing T cells (Th9s) is induced by IL-4 and TGF-β1 or IL-1β. In this article, we report that the transcription factor growth factor-independent 1 transcriptional repressor (GFI1) plays a negative role in mouse Th9 polarization. Moreover, the expression of GFI1 is controlled by liganded RARα, allowing GFI1 to mediate the negative effect of retinoic acid on IL-9 expression. The
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