ArticleImmunology2011
γδT-cell function in sepsis is modulated by C5a receptor signalling.
Article in Immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Targeting complement C5a to improve radiotherapy sensitivity in non-small cell lung cancer.Translational lung cancer research · 2023Article
- [Research advances on the role of complement system activation in post-burn immunity].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Review
- Bruch's Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration.Journal of clinical medicine · 2023Review
- Current Understanding of Osteoimmunology in Certain Osteoimmune Diseases.Frontiers in cell and developmental biology · 2021Review
- Complement activation in obesity, insulin resistance, and type 2 diabetes mellitus.World journal of diabetes · 2020Review
- Significance of Complement System in Ischemic Stroke: A Comprehensive Review.Aging and disease · 2019Review
- Shenfu injection prolongs survival and protects the intestinal mucosa in rats with sepsis by modulating immune response.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2019Article
- Interleukin-17-producing γδ T (γδ17) cells in inflammatory diseases.Immunology · 2018Review
- PI3K/AKT and CD40L Signaling Regulate Platelet Activation and Endothelial Cell Damage in Sepsis.Inflammation · 2018Article
- Osteoimmunology in Bone Fracture Healing.Current osteoporosis reports · 2017Review
- Murine IL-17+ Vγ4 T lymphocytes accumulate in the lungs and play a protective role during severe sepsis.BMC immunology · 2015Article
- C4a: An Anaphylatoxin in Name Only.Journal of innate immunity · 2015Review
- Protein kinase C-δ mediates sepsis-induced activation of complement 5a and urokinase-type plasminogen activator signaling in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
- Complement in immune and inflammatory disorders: pathophysiological mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2013Review
- Regulatory effects of C5a on IL-17A, IL-17F, and IL-23.Frontiers in immunology · 2012Article
- New insights for C5a and C5a receptors in sepsis.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously showed that γδT cells are involved in the pathogenesis of sepsis, but, the underlying mechanisms remained unclear. The present study demonstrates, for the first time, that γδT cells express the complement C5a receptor (C5aR, CD88) and that CD88 expression in γδT cells was up-regulated in mice following sepsis both at protein and mRNA levels. Complement C5a itself contributed to the regulation of C5aR expression on γδT cells, as (i) neutralization of C5a in vivo prevented the expression of C5aR on γδT cells in septic mice and (ii) incubation of mouse spleen cells or purified γδT cells with recombinant C5a in vitro increased CD88 expression by γδT cells at both protein and mRNA levels. C5a receptor on γδT cells also mediates increased interleukin-17 (IL-17) expression as incubation of mouse spleen cells or purified γδT cells with recombinant C5a promotes the IL-17 expression by γδT cells. Ligation of the C5aR on γδT cells activated the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway, which enhances CD88 expression and promotes IL-17 secretion. These results demonstrate that C5a acts directly on the C5aR expressed on γδT cells, resulting in cell activation, and subsequently enhances their capacity for IL-17 production. The up-regulation of the PI3K/Akt pathway following C5a stimulation contributes to up-regulation of γδT-cell function.
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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.