ArticleMucosal immunology2020
Regulatory role of Gpr84 in the switch of alveolar macrophages from CD11b
Article in Mucosal immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 27 citations in OpenAlex.
- Orphan GPR84 facilitates uropod de-adhesion at multiple steps during leukocyte extravasation.EMBO reports · 2026Article
- Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays.Experimental & molecular medicine · 2026Article
- GPR84 aggravates lung inflammation through activating ZBP1-PANoptosome mediated PANoptosis following IAV infection.Cell death discovery · 2026Article
- Medium-Chain Fatty Acid Receptor GPR84 Modulates Cytotoxic CD8 T-cell Antitumor Immunity through Metabolic Reprogramming.Cancer immunology research · 2026Article
- G-Protein-Coupled Receptor 84 Aggravates Early Brain Injury via Microglial NLRP3-ASC Inflammasome After Subarachnoid Hemorrhage.Brain and behavior · 2025Article
- Targeted labeling and depletion of alveolar macrophages using VeDTR mouse technology.iScience · 2025Article
- Mycobacteria Exploit Host GPR84 to Dampen Pro-Inflammatory Responses and Promote Infection in Macrophages.Microorganisms · 2025Article
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- G-protein-coupled receptor 84 regulates acute inflammation in normal and diabetic skin wounds.Cell reports · 2024Article
- Targeting metabolic sensing switch GPR84 on macrophages for cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2024Article
- Regulator of G protein signaling protein 6 alleviates acute lung injury by inhibiting inflammation and promoting cell self-renewal in mice.Cellular & molecular biology letters · 2023Article
- Pro-phagocytic function and structural basis of GPR84 signaling.Nature communications · 2023Article
- Structural insights into ligand recognition and activation of the medium-chain fatty acid-sensing receptor GPR84.Nature communications · 2023Article
- Pro-phagocytic function and structural basis of GPR84 signaling.Research square · 2023Article
- GPR84 signaling promotes intestinal mucosal inflammation via enhancing NLRP3 inflammasome activation in macrophages.Acta pharmacologica Sinica · 2022Article
- Article
- Metabolite transporters as regulators of macrophage polarization.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Metabolite Transporters as Regulators of Immunity.Metabolites · 2020Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute respiratory distress syndrome (ARDS) is a kind of comprehensive disease with excessive inflammation and high clinical mortality. Multiple immune cells are involved in the ARDS process. Amongst these populations, lung-resident alveolar macrophages (AMs) are known to participate in the regulation of ARDS. GPR84, a metabolite-sensing GPCR sensing medium-chain fatty acids (MCFAs), is highly expressed in LPS-challenged macrophages and considered as a pro-inflammatory receptor. In this study, it was hypothesized that Gpr84 may be involved in pulmonary homeostasis via its regulatory effect on the switch of AM status. In LPS-induced ALI mouse model, we identified the internal LPS-induced switch of AMs from CD11b
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.