ArticleCell reports2022
Rapid GPR183-mediated recruitment of eosinophils to the lung after Mycobacterium tuberculosis infection.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Targeting the GPR183/EBI2‒oxysterol axis in tuberculosis: Immunometabolic regulation and prospects for host-directed therapy.Clinical and translational medicine · 2026Review
- Macrophage-derived oxysterols organize T helper 2 cells to suppress type 1 inflammation during pulmonary fungal infection.Science immunology · 2026Article
- Differential Regulation of Oxidative Burst by First Line Drugs Used Against Multi Drug-Resistant Tuberculosis in Naïve Human Innate Immune Cells.Antibiotics (Basel, Switzerland) · 2026Article
- Interstitial and recruited macrophages prevent tuberculosis relapse by limiting immune evasion.EMBO molecular medicine · 2026Article
- Sensing of metabolic signals via GPR183 promotes occupation of lung macrophage niches by monocytes.The Journal of experimental medicine · 2026Article
- High Expression of GPR183 Predicts Poor Survival in Cytogenetically Normal Acute Myeloid Leukemia.Biochemical genetics · 2026Article
- Clinical characteristics of peripheral blood eosinophilia in nontuberculous mycobacterial disease: a multicenter comparative retrospective study.Frontiers in cellular and infection microbiology · 2026Article
- Glucocorticoids suppress early lung inflammation and impair control of SARS-CoV-2 in non-human primates.PloS one · 2026Article
- Diabetes exacerbates myasthenia gravis by enhancing pathological thymic output via the GPR183-7α,25-OHC axis.Journal of neuroinflammation · 2025Article
- Pre-treatment blood cell counts and inflammatory markers predict the radiologic severity of post-tuberculosis lung disease.BMC infectious diseases · 2025Article
- Spatial organization of pulmonary type 2 inflammation by a macrophage-derived cholesterol metabolite.bioRxiv : the preprint server for biology · 2025Article
- Oxysterol-Induced Inflammation in Human Diseases: Strategies for Treatment with Natural Compounds and Synthetic Molecules.Molecules (Basel, Switzerland) · 2025Review
- Article
- A Blood and Biochemical Indicator-Based Prognostic Model Predicting Latent Tuberculosis Infection: A Retrospective Study.Tropical medicine and infectious disease · 2025Article
- A gut commensal protozoan determines respiratory disease outcomes by shaping pulmonary immunity.Cell · 2025Article
- Association between blood inflammatory status and the survival of tuberculosis: a five-year cohort study.Frontiers in immunology · 2025Article
- Identification of diagnostic biomarkers and molecular subtype analysis associated with m6A in Tuberculosis immunopathology using machine learning.Scientific reports · 2024Article
- Spatial adaptation of eosinophils and their emerging roles in homeostasis, infection and disease.Nature reviews. Immunology · 2024Review
- Cholesterol sensing and metabolic adaptation in tissue immunity.Trends in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors at 6 institutions in 3 countries.
Funding
Abstract
Influx of eosinophils into the lungs is typically associated with type II responses during allergy and fungal and parasitic infections. However, we previously reported that eosinophils accumulate in lung lesions during type I inflammatory responses to Mycobacterium tuberculosis (Mtb) in humans, macaques, and mice, in which they support host resistance. Here we show eosinophils migrate into the lungs of macaques and mice as early as one week after Mtb exposure. In mice this influx is CCR3 independent and instead requires cell-intrinsic expression of the oxysterol receptor GPR183, which is highly expressed on human and macaque eosinophils. Murine eosinophils interact directly with bacilli-laden alveolar macrophages, which upregulate the oxysterol-synthesizing enzyme Ch25h, and eosinophil recruitment is impaired in Ch25h-deficient mice. Our findings show that eosinophils are among the earliest cells from circulation to sense and respond to Mtb infection of alveolar macrophages and reveal a role for GPR183 in the migration of eosinophils into lung tissue.
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.