ArticleiScience2025
RGS2 is an innate immune checkpoint for suppressing Gαq-mediated IFNγ generation and lung injury.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Transcriptomic remodeling of bone marrow mesenchymal stromal cells in pediatric B-cell acute lymphoblastic leukemia: a four-gene signature.Translational pediatrics · 2026Article
- ERG-deficient endothelium identifies IL-8/CXCR2 axis as a therapeutic target for resolving neutrophilic lung vascular injury.JCI insight · 2026Article
- Mitochondrial-related biomarkers as the diagnostic markers in sepsis induced acute respiratory distress syndrome.European journal of medical research · 2026Article
- Pancreatic β-cell FFA2 deficiency suppresses multiple low dose streptozotocin induced diabetes in male mice.Communications biology · 2025Article
- Heterogeneous Macrophage Activation in Acute Skeletal Muscle Sterile Injury andInternational journal of molecular sciences · 2025Article
- Targeting BATF2-RGS2 axis reduces T-cell exhaustion and restores anti-tumor immunity.Molecular cancer · 2025Article
- Repolarization of inflammatory macrophages into reparative stage targeting cannabinoid receptor2: a potential perspective to dampen lung injury/ARDS.Frontiers in pharmacology · 2025Review
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Abstract
Interferon gamma (IFNγ), a type II interferon, augments tissue inflammation following infections, leading to lethal acute lung injury (ALI), yet the mechanisms controlling IFNγ generation in the lungs remain elusive. Here, we identified regulator of G protein signaling 2 (RGS2) as a gatekeeper of the lung's IFNγ levels during infections. Deletion of RGS2 sustained an increase in IFNγ levels in macrophages, leading to unresolvable inflammatory lung injury. This response was not seen in RGS2 null chimeric mice receiving wild-type (WT) bone marrow or the RGS2 gene in alveolar macrophages (AMs) or IFNγ-blocking antibody. RGS2 functioned by suppressing Gαq-mediated IFNγ generation and AM inflammatory signaling. Thus, the inhibition of Gαq blocked IFNγ generation in AMs and rewired AM transcriptomes from an inflammatory to a reparative phenotype in RGS2 null mice, pointing to the RGS2-Gαq axis as a potential target for suppressing inflammatory injury.
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