ArticleBMC immunology2008
Mast cell activation is characterized by upregulation of a functional anaphylatoxin C5a receptor.
Article in BMC immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Mast cell proteases and their significance in physiology, pathology, and therapeutic approaches.Pharmacological reviews · 2026Review
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Deletion of Biliverdin Reductase A in Myeloid Cells Promotes Chemokine Expression and Chemotaxis in Part via a Complement C5a--C5aR1 Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- An Inflammation-Centric View of Neurological Disease: Beyond the Neuron.Frontiers in cellular neuroscience · 2018Review
- The Mast Cell, Contact, and Coagulation System Connection in Anaphylaxis.Frontiers in immunology · 2017Review
- Mast cells, glia and neuroinflammation: partners in crime?Immunology · 2014Review
- Mast cell-glia axis in neuroinflammation and therapeutic potential of the anandamide congener palmitoylethanolamide.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2012Review
- Role of C3a receptors, C5a receptors, and complement protein C6 deficiency in collagen antibody-induced arthritis in mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- G protein coupled receptor specificity for C3a and compound 48/80-induced degranulation in human mast cells: roles of Mas-related genes MrgX1 and MrgX2.European journal of pharmacology · 2011Article
- C5a receptor enables participation of mast cells in immune complex arthritis independently of Fcγ receptor modulation.Arthritis and rheumatism · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMast cells (MC) are key effector cells of allergic diseases and resistance to helminthic parasites and induce or amplify diverse innate and adaptive immune responses. The signals controlling MC mobilization during inflammation are not fully understood.
resultsSince anaphylatoxins are attractive candidates as MC chemoattractants, we investigated expression and function of anaphylatoxin receptors in murine MC. Precursor cell-derived MC cultured with IL-3 in the presence or absence of SCF did not express significant amounts of surface C5a receptor (C5aR) or C3a receptor (C3aR). MC required approximately 4 h of stimulation with Ag (DNP-albumin, following preincubation with IgE anti-DNP), ionomycin, or PMA to enable a strong chemotactic response towards C5a, paralleled by a distinct C5aR upregulation. Likewise, C5a induced intracellular calcium fluxes solely in activated MC. In contrast, C3a proved to be a weak MC chemotaxin and unable to increase intracellular calcium. Primary peritoneal MC did not express detectable amounts of anaphylatoxin receptors, however, similar to precursor cell-derived MC, stimulation with Ag or ionomycin for 4 h induced a prominent surface expression of C5aR whereas C3aR remained undetectable.
conclusionCollectively, our results suggest that Ag-dependent as well as -independent activation induces an inflammatory MC phenotype which is distinguished by neoexpression of a functional C5aR as a novel effector mechanism in MC-mediated pathogenesis.
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