ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2012
Evidence for anti-inflammatory effects of C5a on the innate IL-17A/IL-23 axis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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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
48 citing papers in PubMed, 68 citations in OpenAlex.
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- Identification of a genetic region linked to tolerance to MRSA infection using Collaborative Cross mice.PLoS genetics · 2024Article
- Cell-intrinsic C5a synergizes with Dectin-1 in macrophages to mediate fungal killing.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Interleukin 26 Induces Macrophage IL-9 Expression in Rheumatoid Arthritis.International journal of molecular sciences · 2023Article
- Bacterial polyphosphates induce CXCL4 and synergize with complement anaphylatoxin C5a in lung injury.Frontiers in immunology · 2022Article
- Complement receptor C5aR1 on osteoblasts regulates osteoclastogenesis in experimental postmenopausal osteoporosis.Frontiers in endocrinology · 2022Article
- Anaphylatoxins orchestrate Th17 response via interactions between CD16+ monocytes and pleural mesothelial cells in tuberculous pleural effusion.PLoS neglected tropical diseases · 2021Article
- The C5a/C5a receptor 1 axis controls tissue neovascularization through CXCL4 release from platelets.Nature communications · 2021Article
- Targeting Complement C5a Receptor 1 for the Treatment of Immunosuppression in Sepsis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Complement Inhibition and COVID-19: The Story so Far.ImmunoTargets and therapy · 2021Review
- Current understanding of periodontal disease pathogenesis and targets for host-modulation therapy.Periodontology 2000 · 2020Review
- Susceptibility Analysis in Several Mouse Strains Reveals Robust T-Cell Responses AfterFrontiers in cellular and infection microbiology · 2020Article
- CCR2 Mediates Chronic LPS-Induced Pulmonary Inflammation and Hypoalveolarization in a Murine Model of Bronchopulmonary Dysplasia.Frontiers in immunology · 2020Article
- Riemerella anatipestifer infection in ducks induces IL-17A production, but not IL-23p19.Scientific reports · 2019Article
- Mediatory roles of leukotriene BScientific reports · 2019Article
- Kinetics of Physiological and Behavioural Responses in Endotoxemic Pigs with or without Dexamethasone Treatment.International journal of molecular sciences · 2019Article
- Complement-Dependent Mechanisms and Interventions in Periodontal Disease.Frontiers in immunology · 2019Review
- Species-specific differences in regulation of macrophage inflammation by the C3a-C3a receptor axis.Innate immunity · 2018Article
- Emerging role of C5a/C5aR IL-17A axis in cGVHD.American journal of translational research · 2018Article
- IL-17A Produced by Innate Lymphoid Cells Is Essential for Intestinal Ischemia-Reperfusion Injury.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
There is growing evidence that the complement activation product C5a positively or negatively regulates inflammatory functions. The studies presented here report that C5a exerts anti-inflammatory effects by altering production of the cytokines IL-17A and IL-23 during endotoxic shock in young adult male C57BL/6J mice and has similar effects on macrophages from the same mice. IL-17A and IL-23 both appeared in plasma during endotoxemia, and their neutralization improved survival. The relevant sources of IL-17A during endotoxemia were not CD4(+) cells, γδ T cells, or NK cells but CD11b(+)F4/80(+) macrophages. The addition in vitro of C5a to lipopolysaccharide-activated peritoneal macrophages dose dependently antagonized the production of IL-17A (IC(50), 50-100 nM C5a) and IL-23 (IC(50), 10 nM C5a). This suppression required the receptor C5aR, but was independent of the second C5a receptor, C5L2. Genetic absence of C5aR was associated with much higher levels of IL-17A and IL-23 during endotoxic shock. Mechanistically, C5a mediated its effects on the IL-17A/IL-23 axis in a 2-step process. C5a caused activation of the PI3K-Akt and MEK1/2-ERK1/2 pathways, resulting in induction of IL-10, which powerfully inhibited production of IL-17A and IL-23. These data identify previously unknown mechanisms by which the anaphylatoxin C5a limits acute inflammation and antagonizes the IL-17A/IL-23 axis.
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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.