ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Type I IFNs regulate effector and regulatory T cell accumulation and anti-inflammatory cytokine production during T cell-mediated colitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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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Who cites it
57 citing papers in PubMed, 83 citations in OpenAlex.
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- Targeting Impaired Type I Interferon-IL-27 Signaling Rescues T Regulatory Cell Suppressive Function in Relapsing-Remitting Multiple Sclerosis.bioRxiv : the preprint server for biology · 2025Article
- Type I interferons in inflammatory bowel diseases: balancing barrier integrity, repair and inflammation in the intestinal epithelium.Frontiers in medicine · 2025Review
- Cytokine Profile in Predicting the Effectiveness of Advanced Therapy for Ulcerative Colitis: A Narrative Review.Biomedicines · 2024Review
- Increased type-I interferon level is associated with liver damage and fibrosis in primary sclerosing cholangitis.Hepatology communications · 2024Article
- Crosstalk Between Microbiota, Microbial Metabolites, and Interferons in the Inflammatory Bowel Disease Gut.Journal of the Canadian Association of Gastroenterology · 2024Review
- Commensal bacteria promote type I interferon signaling to maintain immune tolerance in mice.The Journal of experimental medicine · 2024Article
- Recent Advances in Cell-Based In Vitro Models to Recreate Human Intestinal Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Cell-penetrating TLR inhibitor peptide alleviates ulcerative colitis by the functional modulation of macrophages.Frontiers in immunology · 2023Article
- Inflammatory Bowel Disease: A Review of Pre-Clinical Murine Models of Human Disease.International journal of molecular sciences · 2022Review
- Gut Barrier Damage and Gut Translocation of Pathogen Molecules in Lupus, an Impact of Innate Immunity (Macrophages and Neutrophils) in Autoimmune Disease.International journal of molecular sciences · 2022Review
- A genetic screen identifies a protective type III interferon response to Cryptosporidium that requires TLR3 dependent recognition.PLoS pathogens · 2022Article
- Effects of a multicomponent microbial feed additive containing prebiotics and probiotics on health, immune status, metabolism, and performance of newly weaned beef steers during a 35-d receiving period.Translational animal science · 2022Article
- Immunoregulatory effects of RGMb in gut inflammation.Frontiers in immunology · 2022Article
- STING Agonist Mitigates Experimental Autoimmune Encephalomyelitis by Stimulating Type I IFN-Dependent and -Independent Immune-Regulatory Pathways.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- A Role of Variance in Interferon Genes to Disease Severity in COVID-19 Patients.Frontiers in genetics · 2021Review
- Interfering With Inflammation: Heterogeneous Effects of Interferons in Graft-Frontiers in immunology · 2021Review
- T Cell-Mediated Immune Responses to AAV and AAV Vectors.Frontiers in immunology · 2021Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
We explored the function of endogenous type I IFNs (IFN-1) in the colon using the T cell adoptive transfer model of colitis. Colon mononuclear phagocytes (MPs) constitutively produced IFN-1 in a Toll/IL-1R domain-containing adapter-inducing IFN-β-dependent manner. Transfer of CD4(+)CD45RB(hi) T cells from wild-type (WT) or IFN-α/β receptor subunit 1 knockout (IFNAR1(-/-)) mice into RAG(-/-) hosts resulted in similar onset and severity of colitis. In contrast, RAG(-/-) × IFNAR1(-/-) double knockout (DKO) mice developed accelerated severe colitis compared with RAG(-/-) hosts when transferred with WT CD4(+)CD45RB(hi) T cells. IFNAR signaling on host hematopoietic cells was required to delay colitis development. MPs isolated from the colon lamina propria of IFNAR1(-/-) mice produced less IL-10, IL-1R antagonist, and IL-27 compared with WT MPs. Accelerated colitis development in DKO mice was characterized by early T cell proliferation and accumulation of CD11b(+)CD103(-) dendritic cells in the mesenteric lymph nodes, both of which could be reversed by systemic administration of IL-1R antagonist (anakinra). Cotransfer of CD4(+)CD25(+) regulatory T cells (Tregs) from WT or IFNAR1(-/-) mice prevented disease caused by CD4(+)CD45RB(hi) T cells. However, WT CD4(+)CD25(+)Foxp3(GFP+) Tregs cotransferred with CD4(+)CD45RB(hi) T cells into DKO hosts failed to expand or maintain Foxp3 expression and gained effector functions in the colon. To our knowledge, these data are the first to demonstrate an essential role for IFN-1 in the production of anti-inflammatory cytokines by gut MPs and the indirect maintenance of intestinal T cell homeostasis by both limiting effector T cell expansion and promoting Treg stability.
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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.