ArticleArthritis and rheumatism2010
C5a receptor enables participation of mast cells in immune complex arthritis independently of Fcγ receptor modulation.
Article in Arthritis and rheumatism, 2010. 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, 40 citations in OpenAlex.
- IL-1β-driven osteoclastogenic Tregs accelerate bone erosion in arthritis.The Journal of clinical investigation · 2021Article
- Novel Strategies to Target Mast Cells in Disease.Journal of innate immunity · 2021Review
- 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
- The Role of Mast Cells in Bone Metabolism and Bone Disorders.Frontiers in immunology · 2020Review
- Review
- Megakaryocytes compensate for Kit insufficiency in murine arthritis.The Journal of clinical investigation · 2017Article
- RANK-Independent Osteoclast Formation and Bone Erosion in Inflammatory Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- Receptor Protein Tyrosine Phosphatase α-Mediated Enhancement of Rheumatoid Synovial Fibroblast Signaling and Promotion of Arthritis in Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2016Article
- A subset of AID-dependent B-1a cells initiates hypersensitivity and pneumococcal pneumonia resistance.Annals of the New York Academy of Sciences · 2015Review
- Article
- Evaluation of synovial mast cell functions in autoimmune arthritis.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Mast cell anaphylatoxin receptor expression can enhance IgE-dependent skin inflammation in mice.The Journal of allergy and clinical immunology · 2013Article
- Neutrophils orchestrate their own recruitment in murine arthritis through C5aR and FcγR signaling.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Article
- Ras guanine nucleotide-releasing protein-4 (RasGRP4) involvement in experimental arthritis and colitis.The Journal of biological chemistry · 2012Article
- Mast Cells are Important Modifiers of Autoimmune Disease: With so Much Evidence, Why is There Still Controversy?Frontiers in immunology · 2012Article
- Article
- IL-17RA signaling amplifies antibody-induced arthritis.PloS one · 2011Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
objectiveMast cells are tissue-resident immune sentinels that are implicated in the pathogenesis of inflammatory joint disease. The aim of this study was to test our hypothesis that complement fragments could be key activators of synovial mast cells in autoimmune arthritis.
methodsIn vivo studies used the murine K/BxN arthritis model, a distal symmetric polyarthritis mediated by IgG immune complexes. Expression of C5aR on synovial mast cells was determined by immunohistochemical and functional studies. C5aR(-/-) and control mast cells were engrafted into mast cell-deficient WBB6 F1-Kit(w) /Kit(W-v) (W/Wv) mice to examine the requirement for this receptor in arthritis. C5aR-dependent activation of mast cells was investigated in C5aR(-/-) animals and in murine and human mast cell cultures.
resultsMurine synovial mast cells express functional C5aR. Unlike their wild-type counterparts, C5aR(-/-) mast cells adoptively transferred into W/Wv mice were not competent to restore arthritis, despite equivalent synovial engraftment. Activation of C5aR(-/-) mast cells by K/BxN serum in vivo remained intact, indicating that C5aR is dispensable for normal IgG-mediated triggering. Consistent with this result, cultured mast cells treated with C5a failed to modulate the expression of Fcγ receptors (FcγR) or to otherwise alter the activation threshold. In human mast cells, C5a promoted the production of the neutrophil chemotaxin interleukin-8, and recruitment of neutrophils at 24 hours after serum administration was impaired in C5aR(-/-) mice, suggesting that enhanced neutrophil chemoattractant production underlies the requirement for C5aR on mast cells in arthritis.
conclusionStimulation via C5aR is required to unleash the proinflammatory activity of synovial mast cells in immune complex arthritis, albeit via a mechanism that is distinct from C5a-modulated expression of FcγR.
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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.