ArticleMucosal immunology2015
The Axl receptor tyrosine kinase is a discriminator of macrophage function in the inflamed lung.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
What it found
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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
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Efferocytosis and inflammation: a bibliometric and systematic analysis.Frontiers in medicine · 2025Pooled it
- AXL mediates influenza A virus entry and drives virus-induced inflammation.Emerging microbes & infections · 2026Article
- Structural organization of TAM receptor ectodomains.The Biochemical journal · 2026Article
- Uncovering immune dysfunction in ACLF: Cellular mechanisms, molecular pathways, and therapeutic frontiers.Journal of hepatology · 2026Review
- Review
- Inhibition of AXL receptor tyrosine kinase increases osteoblast function and bone mass.Bone research · 2026Article
- AXL-dependent autophagy impairment differentiates monocyte-derived macrophages from Crohn's disease and intestinal tuberculosis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026Article
- Microbiota-induced EI24 improves homeostasis but impedes function of alveolar macrophages via metabolic regulation.Nature communications · 2026Article
- Machine learning and bioinformatics framework integration reveal potential characteristic genes related to immune cell infiltration in post-traumatic stress disorder.Scientific reports · 2025Article
- Monocyte-derived macrophages support alveolar regeneration via oncostatin M post-H1N1 infection during the recovery phase.Respiratory research · 2025Article
- The spleen tyrosine kinase inhibitor entospletinib resolves inflammation to promote repair following acute kidney injury.JCI insight · 2025Article
- Royal jelly fermented by honeybee queen (Apis mellifera)-derived Lactobacillus panisapium M1 enhances macrophage phagocytosis through the TLR2/MAPK/SR signaling pathway.BMC complementary medicine and therapies · 2025Article
- Geranylgeranyl diphosphate synthase deficiency impairs efferocytosis and resolution of acute lung injury.Respiratory research · 2025Article
- Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025Review
- Review
- Dys-regulated phosphatidylserine externalization as a cell intrinsic immune escape mechanism in cancer.Cell communication and signaling : CCS · 2025Review
- AXL: shapers of tumor progression and immunosuppressive microenvironments.Molecular cancer · 2025Review
- Article
- AXL as immune regulator and therapeutic target in Acute Myeloid Leukemia: from current progress to novel strategies.Experimental hematology & oncology · 2024Review
- Diagnosis of Pleural Mesothelioma: Is Everything Solved at the Present Time?Current oncology (Toronto, Ont.) · 2024Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Much of the biology surrounding macrophage functional specificity has arisen through examining inflammation-induced polarizing signals, but this also occurs in homeostasis, requiring tissue-specific environmental triggers that influence macrophage phenotype and function. The TAM receptor family of receptor tyrosine kinases (Tyro3, Axl and MerTK) mediates the non-inflammatory removal of apoptotic cells by phagocytes through the bridging phosphatidylserine-binding molecules growth arrest-specific 6 (Gas6) or Protein S. We show that one such TAM receptor (Axl) is exclusively expressed on mouse airway macrophages, but not interstitial macrophages and other lung leukocytes, under homeostatic conditions and is constitutively ligated to Gas6. Axl expression is potently induced by granulocyte-macrophage colony-stimulating factor expressed in the healthy and inflamed airway, and by type I interferon or Toll-like receptor-3 stimulation on human and mouse macrophages, indicating potential involvement of Axl in apoptotic cell removal under inflammatory conditions. Indeed, an absence of Axl does not cause sterile inflammation in health, but leads to exaggerated lung inflammatory disease upon influenza infection. These data imply that Axl allows specific identification of airway macrophages, and that its expression is critical for macrophage functional compartmentalization in the airspaces or lung interstitium. We propose that this may be a critical feature to prevent excessive inflammation because of secondary necrosis of apoptotic cells that have not been cleared by efferocytosis.
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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.