ArticleThe Journal of clinical investigation2004
The anaphylatoxin C3a downregulates the Th2 response to epicutaneously introduced antigen.
Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 75 citations in OpenAlex.
- The Complement System.Advances in experimental medicine and biology · 2025Review
- Article
- The role of complement in nonalcoholic fatty liver disease.Frontiers in immunology · 2022Review
- Complement Component C3: A Novel Biomarker Participating in the Pathogenesis of Non-alcoholic Fatty Liver Disease.Frontiers in medicine · 2021Review
- Species-specific differences in regulation of macrophage inflammation by the C3a-C3a receptor axis.Innate immunity · 2018Article
- Article
- The Anaphylatoxin C3a Receptor Expression on Human M2 Macrophages Is Down-Regulated by Stimulating the Histamine H4 Receptor and the IL-4 Receptor.Journal of innate immunity · 2018Article
- Immune recognition of salivary proteins from the cattle tick Rhipicephalus microplus differs according to the genotype of the bovine host.Parasites & vectors · 2017Article
- Complement activation in the context of stem cells and tissue repair.World journal of stem cells · 2015Review
- Variation in the Ovine Abomasal Lymph Node Transcriptome between Breeds Known to Differ in Resistance to the Gastrointestinal Nematode.PloS one · 2015Article
- Renal C3 complement component: feed forward to diabetic kidney disease.American journal of nephrology · 2015Article
- The receptor for the complement C3a anaphylatoxin (C3aR) provides host protection against Listeria monocytogenes-induced apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Complement anaphylatoxins as immune regulators in cancer.Cancer medicine · 2014Review
- C3a receptor promotes viral containment in mice inoculated with vaccinia virus at sites of allergic skin inflammation.The Journal of allergy and clinical immunology · 2013Article
- Article
- Dysregulation of complement system and CD4+ T cell activation pathways implicated in allergic response.PloS one · 2013Article
- Gene expression profiling in acute allograft rejection: challenging the immunologic constant of rejection hypothesis.Journal of translational medicine · 2011Article
- A complex role for complement in allergic asthma.Expert review of clinical immunology · 2010Review
- Complement activation by CpG in a human whole blood loop system: mechanisms and immunomodulatory effects.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- A protective role for C5a in the development of allergic asthma associated with altered levels of B7-H1 and B7-DC on plasmacytoid dendritic cells.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Mechanical injury to the skin results in activation of the complement component C3 and release of the anaphylatoxin C3a. C3a binds to a seven-transmembrane G protein-coupled receptor, C3aR. We used C3aR(-/-) mice to examine the role of C3a in a mouse model of allergic inflammation induced by epicutaneous sensitization with OVA. C3aR(-/-) mice exhibited an exaggerated Th2 response to epicutaneous but not to intraperitoneal sensitization with OVA, as evidenced by significantly elevated levels of serum OVA-specific IgG1 and significantly increased secretion of the Th2 cytokines IL-4, IL-5, and IL-10 by antigen-stimulated splenocytes. Presentation of OVA peptide by C3aR(-/-) APCs caused significantly more IL-4 and IL-5 secretion by T cells from OVA-T cell receptor (OVA-TCR) transgenic mice compared with presentation by WT APCs. C3a inhibited the ability of splenocytes, but not of highly purified T cells, to secrete Th2 cytokines in response to TCR ligation. This inhibition was mediated by IL-12 secreted by APCs in response to C3a. These results suggest that C3a-C3aR interactions inhibit the ability of APCs to drive Th2 cell differentiation in response to epicutaneously introduced antigen and may have important implications for allergic skin diseases.
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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.