ArticleCytokine2022
Interferon gamma upregulates the cytokine receptors IFNGR1 and TNFRSF1A in HT-29-MTX E12 cells.
Article in Cytokine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Prostate tumor-mediated IFNG signaling primes myeloid cells in bone premetastatic niche for immunosuppressive IL-10 signaling.The Journal of clinical investigation · 2025Article
- Mucosal Responses to Type II Interferon in IBD.Inflammatory bowel diseases · 2025Article
- Leveraging Organ-on-Chip Models to Investigate Host-Microbiota Dynamics and Targeted Therapies for Inflammatory Bowel Disease.Advanced healthcare materials · 2025Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The intestinal mucosa protects the body from physical damage, pathogens, and antigens. However, inflammatory bowel diseases (IBDs) patients suffer from poor mucosal tissue function, including the lack of an effective cellular and/or mucus barrier. We investigated the mucus producing human colonic epithelial cell line HT29-MTX E12 to study its suitability as an in vitro model of cell/mucus barrier adaption during IBD. It was found that the proinflammatory cytokine interferon-gamma (IFN-γ), but not tumor necrosis factor-alpha (TNF-α), reduced cell viability. IFN-γ and TNF-α were found to synergize to decrease barrier function, as measured by trans-epithelial electric resistance (TER) and molecular flux assays. Cells cultured under an air-liquid interface produced an adherent mucus layer, and under these conditions reduced barrier function was found after cytokine exposure. Furthermore, IFN-γ, but not TNF-α treatment, upregulated the IFN-γ receptor 1 (IFNGR1) and TNF-α receptor super family 1A (TNFRSF1A) subunit mRNA in vitro. Co-stimulation resulted in increased mRNA expression of CLDN 2 and 5, two gene known to play a role in epithelial barrier integrity. Analysis of IBD patient samples revealed IFNGR1 and TNFRSF mRNA increased coincidently with guanylate binding protein 1 (GBP1) expression, an indicator of NFkB activity. Lastly, CLDN2 was found at higher levels in IBD patients while HNF4a was suppressed with disease. In conclusion, IFN-γ and TNF-α degrade epithelial/mucus barriers coincident with changes in CLDN gene and cytokine receptor subunit mRNA expression in HT29-MTX E12 cells. These changes largely reflect those observed in IBD patient samples.
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Registered trials
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