ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Mast cells contribute to autoimmune inflammatory arthritis via their tryptase/heparin complexes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 157 citations in OpenAlex.
- Mast cell proteases and their significance in physiology, pathology, and therapeutic approaches.Pharmacological reviews · 2026Review
- Immunosuppressive Cyclotides: A Promising Approach for Treating Autoimmune Diseases.The protein journal · 2024Review
- GW0742 reduces mast cells degranulation and attenuates neurological impairments via PPARExperimental neurology · 2024Article
- Mast cells as important regulators in the development of psoriasis.Frontiers in immunology · 2022Review
- Neuroimmune connections between corticotropin-releasing hormone and mast cells: novel strategies for the treatment of neurodegenerative diseases.Neural regeneration research · 2021Review
- Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications.Frontiers in immunology · 2021Review
- The association between synovial fluid serine proteinase activity and response to intra-articular corticosteroid injection in psoriatic arthritis.Clinical rheumatology · 2020Article
- The Role of Mast Cells in Bone Metabolism and Bone Disorders.Frontiers in immunology · 2020Review
- Roles of mast cells in rheumatoid arthritis.The Korean journal of internal medicine · 2020Review
- Mast cells as a unique hematopoietic lineage and cell system: From Paul Ehrlich's visions to precision medicine concepts.Theranostics · 2020Review
- Paradigm Shifts in Mast Cell and Basophil Biology and Function: An Emerging View of Immune Regulation in Health and Disease.Methods in molecular biology (Clifton, N.J.) · 2020Review
- IgE-mediated mast cell activation promotes inflammation and cartilage destruction in osteoarthritis.eLife · 2019Article
- Mast Cells in Early Rheumatoid Arthritis.International journal of molecular sciences · 2019Review
- Diverse exocytic pathways for mast cell mediators.Biochemical Society transactions · 2018Review
- Munc13 proteins control regulated exocytosis in mast cells.The Journal of biological chemistry · 2018Article
- A Novel, Nonpeptidic, Orally Active Bivalent Inhibitor of Human β-Tryptase.Pharmacology · 2018Article
- Potential Role of Cytochrome c and Tryptase in Psoriasis and Psoriatic Arthritis Pathogenesis: Focus on Resistance to Apoptosis and Oxidative Stress.Frontiers in immunology · 2018Review
- A novel method to identify hub pathways of rheumatoid arthritis based on differential pathway networks.Molecular medicine reports · 2017Article
- Peroxisome proliferator-activated receptor γ agonist suppresses mast cell maturation and induces apoptosis.Molecular medicine reports · 2017Article
- Effect of tryptase inhibition on joint inflammation: a pharmacological and lentivirus-mediated gene transfer study.Arthritis research & therapy · 2017Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Although mast cells (MCs) often are abundant in the synovial tissues of patients with rheumatoid arthritis, the contribution of MCs to joint inflammation and cartilage loss remains poorly understood. MC-restricted tryptase/heparin complexes have proinflammatory activity, and significant amounts of human tryptase beta (hTryptase-beta) are present in rheumatoid arthritis synovial fluid. Mouse MC protease-6 (mMCP-6) is the ortholog of hTryptase-beta, and this serine protease is abundant in the synovium of arthritic mice. We now report that C57BL/6 (B6) mice lacking their tryptase/heparin complexes have attenuated arthritic responses, with mMCP-6 as the dominant tryptase responsible for augmenting neutrophil infiltration in the K/BxN mouse serum-transfer arthritis model. While inflammation in this experimental arthritis model was not dependent on protease-activated receptor-2, it was dependent on the chemokine receptor CXCR2. In support of the latter data, exposure of synovial fibroblasts to hTryptase-beta/heparin or mMCP-6/heparin complexes resulted in expression of the neutrophil chemotactic factors CXCL1/KC, CXCL5/LIX, and CXCL8/IL-8. Our proteomics, histochemistry, and immunohistochemistry data also revealed substantial loss of cartilage-derived aggrecan proteoglycans in the arthritic joints of wild-type B6 mice but not mMCP-6-null B6 mice. These observations demonstrate the functional contribution of MC-restricted tryptase/heparin complexes in the K/BxN mouse arthritis model and connect our mouse findings with rheumatoid arthritis pathophysiology.
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