ArticleImmunology2004
Human monocyte-derived dendritic cells are chemoattracted to C3a after up-regulation of the C3a receptor with interferons.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
20 citing papers in PubMed, 61 citations in OpenAlex.
- Review
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.International journal of molecular sciences · 2024Review
- Complement protein C3a enhances adaptive immune responses towards FVIII products.Haematologica · 2023Article
- Complement activation products in the circulation and urine of primary membranous nephropathy.BMC nephrology · 2019Article
- Comparative Transcriptomic Analysis Identifies a Range of Immunologically Related Functional Elaborations of Lymph Node Associated Lymphatic and Blood Endothelial Cells.Frontiers in immunology · 2019Article
- C3a is required for ILC2 function in allergic airway inflammation.Mucosal immunology · 2018Article
- Decoding the chemotactic signal.Journal of leukocyte biology · 2018Review
- Complement Activation in Liver Transplantation: Role of Donor Macrosteatosis and Implications in Delayed Graft Function.International journal of molecular sciences · 2018Review
- 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
- Activation of the complement cascade enhances motility of leukemic cells by downregulating expression of HO-1.Leukemia · 2017Article
- Complement anaphylatoxins as immune regulators in cancer.Cancer medicine · 2014Review
- Negative regulation of pulmonary Th17 responses by C3a anaphylatoxin during allergic inflammation in mice.PloS one · 2012Article
- Functional modulation of human monocytes derived DCs by anaphylatoxins C3a and C5a.Immunobiology · 2012Article
- Plasma proteomic analysis of simian immunodeficiency virus infection of rhesus macaques.Journal of proteome research · 2010Article
- Regulation of human mast cell and basophil function by anaphylatoxins C3a and C5a.Immunology letters · 2010Review
- The role of the anaphylatoxins in health and disease.Molecular immunology · 2009Review
- C3a receptor antagonist attenuates brain injury after intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2009Article
- Anaphylatoxin C3a receptors in asthma.Respiratory research · 2005Review
- The anaphylatoxin C3a downregulates the Th2 response to epicutaneously introduced antigen.The Journal of clinical investigation · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anaphylatoxin C3a is an important inflammatory mediator in the innate and adaptive immune systems. Recent reports in various animal models have fostered the role of C3a in mediating allergic reactions such as pulmonary allergies. However, data in humans are limited and the cellular targets for C3a are not fully understood. We sought to explore human dendritic cells as a new target for C3a, because C3a receptor (C3aR) expression has been described on myeloid cells, and dendritic cells are likely make contact with C3a at sites of inflammatory reactions. In this study, we demonstrated the expression of the C3aR on human monocyte-derived dendritic cells (MoDC) and its up-regulation by interferon (IFN)-alpha, IFN-gamma and prostaglandin E2 (PGE2). The strongest up-regulation was yielded by the combination of IFN-alpha+ IFN-gamma. Tumour necrosis factor-alpha (TNF-alpha) down-regulated the C3aR. After up-regulation of the C3aR by IFN-alpha+ IFN-gamma, C3a significantly up-regulated the surface expression of CD54, CD83 and CD86, but not of CD40, CD80 or human leucocyte antigen (HLA)-DR. C3a had no effect on the production of interleukin (IL)-10 or IL-12p70, or on the capacity of MoDC to stimulate autologous T-cell proliferation. However, C3a had a direct migratory effect on MoDC, as indicated by the induction of F-actin polymerization and migration in Boyden chamber experiments, which was pronounced after up-regulation of the C3aR with IFN-alpha+ IFN-gamma. Therefore, dendritic cells represent another group of target cells that might be recruited by C3a to areas of inflammation, in particular under conditions where IFNs are increased in the surrounding environment.
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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.