ArticleRheumatology (Oxford, England)2021
Mer tyrosine kinase as a possible link between resolution of inflammation and tissue fibrosis in IgG4-related disease.
Article in Rheumatology (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Single-cell RNA sequencing and high-dimensional flow cytometry reveal distinct peripheral immune landscapes of type 1 autoimmune pancreatitis and pancreatic ductal adenocarcinoma.Clinical and translational medicine · 2026Article
- Macrophages Are Critical Inducers of Bleomycin-Induced Fibrosis in a Systemic Scleroderma Model.The American journal of pathology · 2026Article
- Beyond the Th2 paradigm: CD4+ cytotoxic T lymphocytes as key drivers of tissue damage and fibrosis in IgG4-related disease.Frontiers in immunology · 2026Review
- The role of macrophage polarization in organ transplantation: research progress on impact on graft injury, repair, and fibrosis.Frontiers in immunology · 2026Review
- IgG4-Related Disease: Emerging Roles of Novel Genetic Variants, Immune Cell Subsets and Therapeutic Targets.Allergy · 2025Review
- IgG4-related disease and other fibro-inflammatory conditions.Nature reviews. Rheumatology · 2025Review
- LGR6 modulates intervertebral disc degeneration through regulation of macrophage efferocytosis.Journal of translational medicine · 2025Article
- Distinct TYRO3 and PROS1 expression levels contribute to preeclampsia pathogenesis.Histochemistry and cell biology · 2025Article
- Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025Review
- Ovarian expression of MerTK and its ligand Pros1 in non-pregnant estrus and pregnant mice.Journal of molecular histology · 2024Article
- Osteopontin regulation of MerTKiScience · 2024Article
- Immune dysregulation in immunoglobulin G4-related disease.The Japanese dental science review · 2023Review
- Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023Review
- Editorial: The key role of Mer receptor tyrosine kinase: where inflammation ends and fibrosis begins.Frontiers in immunology · 2023Article
- Elevated expression of TAM receptor tyrosine kinase in synovial fluid and synovial tissue of rheumatoid arthritis.Clinical and experimental immunology · 2022Article
- Pomegranate Peel Extract Decreases Plaque Necrosis and Advanced Atherosclerosis Progression inFrontiers in pharmacology · 2022Article
- Research progress on inflammatory mechanism of primary Sjögren syndrome.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
objectivesIgG4-related disease (IgG4-RD) is a systemic fibro-inflammatory disorder characterized by a dysregulated resolution of inflammation and wound healing response that might develop after an apoptotic insult induced by cytotoxic T lymphocytes (CTLs). Mer receptor tyrosine kinase (MerTK) and its ligand, protein S (ProS1), have a pivotal role in the resolution of inflammation, being implicated in the clearance of apoptotic cells, quenching of the immune response and development of tissue fibrosis. In the present work we aimed to investigate a possible involvement of the MerTK signalling pathway in the pathogenesis of IgG4-RD and development of tissue fibrosis.
methodsMerTK and ProS1 expression patterns in IgG4-RD lesions were evaluated by immunohistochemistry and immunofluorescence studies. Circulating MerTK+ monocytes, soluble Mer and MerTK ligands were measured in the peripheral blood of IgG4-RD patients and healthy controls by flow cytometry and ELISA, respectively.
resultsMerTK was highly expressed by macrophages infiltrating IgG4-RD lesions. MerTK+ macrophages were more abundant in IgG4-RD than in Sjögren's syndrome and interacted with apoptotic cells and ProS1-expressing T and B lymphocytes. Moreover, they expressed the pro-fibrotic cytokine TGF-β and their numbers declined following rituximab-induced disease remission. Circulating MerTK+ monocytes, soluble Mer and MerTK ligands were not increased in the peripheral blood of patients with IgG4-RD.
conclusionsThe MerTK-ProS1 axis is activated in IgG4-RD lesions, possibly leading to persistent stimulation of processes involved in the resolution of inflammation and tissue fibrosis.
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Registered trials
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