ArticleImmunology2014
miR-155 deficiency protects mice from experimental colitis by reducing T helper type 1/type 17 responses.
Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.
- Role of miR-155 in inflammatory autoimmune diseases: a comprehensive review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Histopathological Characterization and Differential Expression of miRNAs in Male Pediatric Patients With Lichen Sclerosus.Andrology · 2026Article
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- Article
- Importance of Fecal Microbiota Transplantation and Molecular Regulation as Therapeutic Strategies in Inflammatory Bowel Diseases.Nutrients · 2024Review
- DJ-X-013 reduces LPS-induced inflammation, modulates Th17/ myeloid-derived suppressor cells, and alters NF-κB expression to ameliorate experimental colitis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- microRNA-mRNA Networks Linked to Inflammation and Immune System Regulation in Inflammatory Bowel Disease.Biomedicines · 2024Article
- Article
- Inhibition of microRNA-34c reduces detrusor ROCK2 expression and urinary bladder inflammation in experimental cystitis.Life sciences · 2024Article
- Sea Cucumber Peptide Alleviates Ulcerative Colitis Induced by Dextran Sulfate Sodium by Alleviating Gut Microbiota Imbalance and Regulating miR-155/SOCS1 Axis in Mice.Foods (Basel, Switzerland) · 2023Article
- Updated immunomodulatory roles of gut flora and microRNAs in inflammatory bowel diseases.Clinical and experimental medicine · 2023Review
- Expression Profile of miR-199a and Its Role in the Regulation of Intestinal Inflammation.Animals : an open access journal from MDPI · 2023Article
- MicroRNA: Crucial modulator in purinergic signalling involved diseases.Purinergic signalling · 2023Review
- MicroRNA-155-5p inhibition alleviates irritable bowel syndrome by increasing claudin-1 and ZO-1 expression.Annals of translational medicine · 2023Article
- miRNA Molecules-Late Breaking Treatment for Inflammatory Bowel Diseases?International journal of molecular sciences · 2023Review
- MiRNA-374b-5p and miRNA-106a-5p are related to inflammatory bowel disease via regulating IL-10 and STAT3 signaling pathways.BMC gastroenterology · 2022Article
- miRNA effects on gut homeostasis: therapeutic implications for inflammatory bowel disease.Trends in immunology · 2022Review
- MYC-mediated silencing of miR-181a-5p promotes pathogenic Th17 responses by modulating AKT3-FOXO3 signaling.iScience · 2022Article
- Apigenin Targets MicroRNA-155, Enhances SHIP-1 Expression, and Augments Anti-Tumor Responses in Pancreatic Cancer.Cancers · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Inflammatory bowel disease (IBD), a chronic intestinal inflammatory condition that affects millions of people worldwide, results in high morbidity and exorbitant health-care costs. The critical features of both innate and adaptive immunity are to control inflammation and dysfunction in this equilibrium is believed to be the reason for the development of IBD. miR-155, a microRNA, is up-regulated in various inflammatory disease states, including IBD, and is a positive regulator of T-cell responses. To date, no reports have defined a function for miR-155 with regard to cellular responses in IBD. Using an acute experimental colitis model, we found that miR-155(-/-) mice, as compared to wild-type control mice, have decreased clinical scores, a reversal of colitis-associated pathogenesis, and reduced systemic and mucosal inflammatory cytokines. The increased frequency of CD4+ lymphocytes in the spleen and lamina propria with dextran sodium sulphate induction was decreased in miR-155(-/-) mice. Similarly, miR-155 deficiency abrogated the increased numbers of interferon-γ expressing CD4+ T cells typically observed in wild-type mice in this model. The frequency of systemic and mucosal T helper type 17-, CCR9-expressing CD4+ T cells was also reduced in miR-155(-/-) mice compared with control mice. These findings strongly support a role for miR-155 in facilitating pro-inflammatory cellular responses in this model of IBD. Loss of miR-155 also results in decreases in T helper type 1/type 17, CD11b+) and CD11c+ cells, which correlated with reduced clinical scores and severity of disease. miR-155 may serve as a potential therapeutic target for the treatment of IBD.
Indexed as
Identifiers
What OpenQuestion holds
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.