ArticleJournal of immunology (Baltimore, Md. : 1950)2016
G2A Signaling Dampens Colitic Inflammation via Production of IFN-γ.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Immune Stimulation Using a Gut Microbe-Based Immunotherapy Reduces Disease Pathology and Improves Barrier Function in Ulcerative Colitis.Frontiers in immunology · 2018Trial
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- Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation.Theranostics · 2026Review
- The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.Journal of advanced research · 2025Review
- Targeting Lactate: An Emerging Strategy for Macrophage Regulation in Chronic Inflammation and Cancer.Biomolecules · 2024Review
- Linoleoyl-lysophosphatidylcholine suppresses immune-related adverse events due to immune checkpoint blockade.medRxiv : the preprint server for health sciences · 2024Article
- Non-professional efferocytosis of Salmonella-infected intestinal epithelial cells in the neonatal host.The Journal of experimental medicine · 2024Article
- Efferocytosis by macrophages in physiological and pathological conditions: regulatory pathways and molecular mechanisms.Frontiers in immunology · 2024Review
- Origin and Function of Monocytes in Inflammatory Bowel Disease.Journal of inflammation research · 2024Review
- Mucosal and Plasma Metabolomes in New-onset Paediatric Inflammatory Bowel Disease: Correlations with Disease Characteristics and Plasma Inflammation Protein Markers.Journal of Crohn's & colitis · 2023Article
- IBD-associated G protein-coupled receptor 65 variant compromises signalling and impairs key functions involved in inflammation.Cellular signalling · 2022Article
- Critical roles of G protein-coupled receptors in regulating intestinal homeostasis and inflammatory bowel disease.Mucosal immunology · 2022Review
- Lactate Metabolism-Associated lncRNA Pairs: A Prognostic Signature to Reveal the Immunological Landscape and Mediate Therapeutic Response in Patients With Colon Adenocarcinoma.Frontiers in immunology · 2022Article
- Lysophosphatidylcholine aggravates contact hypersensitivity by promoting neutrophil infiltration and IL17 expression.BMB reports · 2021Article
- Lactate-Dependent Regulation of Immune Responses by Dendritic Cells and Macrophages.Frontiers in immunology · 2021Review
- Efferocytosis in the Central Nervous System.Frontiers in cell and developmental biology · 2021Review
- The Lipid Receptor G2A (GPR132) Mediates Macrophage Migration in Nerve Injury-Induced Neuropathic Pain.Cells · 2020Article
- The clearance of dead cells by efferocytosis.Nature reviews. Molecular cell biology · 2020Review
- Roles of G protein-coupled receptors in inflammatory bowel disease.World journal of gastroenterology · 2020Review
- Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Proinflammatory consequences have been described for lysophosphatidylcholine, a lipid product of cellular injury, signaling via the G protein-coupled receptor G2A on myeloid and lymphoid inflammatory cells. This prompted the hypothesis that genetic deletion of G2A would limit intestinal inflammation in a mouse model of colitis induced by dextran sodium sulfate. Surprisingly, G2A(-/-) mice exhibited significantly worsened colitis compared with wild-type mice, as demonstrated by disease activity, colon shortening, histology, and elevated IL-6 and IL-5 in colon tissues. Investigation of inflammatory cells recruited to inflamed G2A(-/-) colons showed significantly more TNF-α(+) and Ly6C(hi)MHCII(-) proinflammatory monocytes and eosinophils than in wild-type colons. Both monocytes and eosinophils were pathogenic as their depletion abolished the excess inflammation in G2A(-/-) mice. G2A(-/-) mice also had less IFN-γ in inflamed colon tissues than wild-type mice. Fewer CD4(+) lymphocytes were recruited to inflamed G2A(-/-) colons, and fewer colonic lymphocytes produced IFN-γ upon ex vivo stimulation. Administration of IFN-γ to G2A(-/-) mice during dextran sodium sulfate exposure abolished the excess colitic inflammation and reduced colonic IL-5 and eosinophil numbers to levels seen in wild-type mice. Furthermore, IFN-γ reduced the numbers of TNF-α(+) monocyte and enhanced their maturation from Ly6C(hi)MHCII(-) to Ly6C(int)MHCII(+) Taken together, the data suggest that G2A signaling serves to dampen intestinal inflammation via the production of IFN-γ, which, in turn, enhances monocyte maturation to a less inflammatory program and ultimately reduces eosinophil-induced injury of colonic tissues.
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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.