ArticlePloS one2014
Interleukin-17 induces an atypical M2-like macrophage subpopulation that regulates intestinal inflammation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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
46 citing papers in PubMed, 63 citations in OpenAlex.
- Associations between clinical features and therapy with macrophage subpopulations and T cells in inflammatory lesions in the aorta from patients with Takayasu arteritis.Clinical and experimental immunology · 2020Trial
- CXCL5 is associated with neutrophil-driven intestinal inflammation and IL-17-associated epithelial signaling in inflammatory bowel disease.Scientific reports · 2026Article
- Mucosal-associated invariant T cells and the gut-kidney axis: a review.Clinical kidney journal · 2026Review
- Th17/treg balance in Inflammatory Bowel Disease: the role of microbial, and genetic regulators in disease modulation.Frontiers in cell and developmental biology · 2026Review
- Multifaceted Roles of IL-26 in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- Streptococcus gallolyticus supernatant induces M2 macrophage polarization and activates IL-17 F signaling in colorectal tumorigenesis.Gut pathogens · 2025Article
- A review of gut failure as a cause and consequence of critical illness.Critical care (London, England) · 2025Review
- Immune dysregulation in ulcerative colitis: pathogenic mechanisms and therapeutic strategies of traditional Chinese medicine.Frontiers in cell and developmental biology · 2025Review
- The mononuclear phagocyte system obscures the accurate diagnosis of infected joint replacements.Journal of translational medicine · 2024Article
- Review
- TH17 cell: a double-edged sword in the development of inflammatory bowel disease.Therapeutic advances in gastroenterology · 2024Review
- RETRACTED: Aggravation of TGFβ1-Smad Pathway and Autoimmune Myocarditis by Fungicide (Tebuconazole) Exposure.International journal of molecular sciences · 2023Article
- Regulatory Effects of Three-Dimensional Cultured Lipopolysaccharide-Pretreated Periodontal Ligament Stem Cell-Derived Secretome on Macrophages.International journal of molecular sciences · 2023Article
- Roles of macrophages on ulcerative colitis and colitis-associated colorectal cancer.Frontiers in immunology · 2023Review
- The role of Th17 cells in inflammatory bowel disease and the research progress.Frontiers in immunology · 2022Review
- Review
- Analysis of peripheral inflammatory T cell subsets and their effector function in patients with Birdshot Retinochoroiditis.Scientific reports · 2021Article
- IL17A Depletion Affects the Metabolism of Macrophages Treated with Gemcitabine.Antioxidants (Basel, Switzerland) · 2021Article
- T helper 17 cells in the pathophysiology of acute and chronic kidney disease.Kidney research and clinical practice · 2021Article
- Macrophage Heterogeneity in the Intestinal Cells of Salmon: Hints From Transcriptomic and Imaging Data.Frontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin 17 (IL-17) is a pleiotropic cytokine that acts on both immune and non-immune cells and is generally implicated in inflammatory and autoimmune diseases. Although IL-17 as well as their source, mainly but not limited to Th17 cells, is also abundant in the inflamed intestine, the role of IL-17 in inflammatory bowel disease remains controversial. In the present study, by using IL-17 knockout (KO) mice, we investigated the role of IL-17 in colitis, with special focus on the macrophage subpopulations. Here we show that IL-17KO mice had increased susceptibility to DSS-induced colitis which was associated with decrease in expression of mRNAs implicated in M2 and/or wound healing macrophages, such as IL-10, IL-1 receptor antagonist, arginase 1, cyclooxygenase 2, and indoleamine 2,3-dioxygenase. Lamina propria leukocytes from inflamed colon of IL-17KO mice contained fewer CD11b+Ly6C+MHC Class II+ macrophages, which were derived, at least partly, from blood monocytes, as compared to those of WT mice. FACS-purified CD11b+ cells from WT mice, which were more abundant in Ly6C+MHC Class II+ cells, expressed increased levels of genes associated M2/wound healing macrophages and also M1/proinflammatory macrophages. Depletion of this population by topical administration of clodronate-liposome in the colon of WT mice resulted in the exacerbation of colitis. These results demonstrate that IL-17 confers protection against the development of severe colitis through the induction of an atypical M2-like macrophage subpopulation. Our findings reveal a previously unappreciated mechanism by which IL-17 exerts a protective function in colitis.
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.