ArticleThe Journal of clinical investigation2006
Cell-derived anaphylatoxins as key mediators of antibody-dependent type II autoimmunity in mice.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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49 citing papers in PubMed, 120 citations in OpenAlex.
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- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Article
- The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Differential expression of C5aR1 and C5aR2 in innate and adaptive immune cells located in early skin lesions of bullous pemphigoid patients.Frontiers in immunology · 2022Article
- There Is Strength in Numbers: Quantitation of Fc Gamma Receptors on Murine Tissue-Resident Macrophages.International journal of molecular sciences · 2021Article
- Complement System: a Neglected Pathway in Immunotherapy.Clinical reviews in allergy & immunology · 2020Review
- Complement activation in obesity, insulin resistance, and type 2 diabetes mellitus.World journal of diabetes · 2020Review
- Effects of complement and serum IgG on rituximab-dependent natural killer cell-mediated cytotoxicity against Raji cells.Oncology letters · 2019Article
- AGI-134: a fully synthetic α-Gal glycolipid that converts tumors into in situ autologous vaccines, induces anti-tumor immunity and is synergistic with an anti-PD-1 antibody in mouse melanoma models.Cancer cell international · 2019Article
- Complements are involved in alcoholic fatty liver disease, hepatitis and fibrosis.World journal of hepatology · 2018Review
- Brain microvascular endothelial cells exhibit lower activation of the alternative complement pathway than glomerular microvascular endothelial cells.The Journal of biological chemistry · 2018Article
- Abrogation of immune complex glomerulonephritis by native carboxypeptidase and pharmacological antagonism of the C5a receptor.Cellular & molecular immunology · 2016Article
- Cooperative and alternate functions for STIM1 and STIM2 in macrophage activation and in the context of inflammation.Immunity, inflammation and disease · 2015Article
- Genomic regulation of senescence and innate immunity signaling in the retinal pigment epithelium.Mammalian genome : official journal of the International Mammalian Genome Society · 2015Article
- The perfect storm: HLA antibodies, complement, FcγRs, and endothelium in transplant rejection.Trends in molecular medicine · 2015Review
- Differential regulation of proinflammatory mediators following LPS- and ATP-induced activation of monocytes from patients with antiphospholipid syndrome.BioMed research international · 2015Article
- Update on crescentic glomerulonephritis.Seminars in immunopathology · 2014Review
- Siglec-5 and Siglec-14 are polymorphic paired receptors that modulate neutrophil and amnion signaling responses to group B Streptococcus.The Journal of experimental medicine · 2014Article
- Fcγ receptor upregulation is associated with immune complex inflammation in the mouse retina and early age-related macular degeneration.Investigative ophthalmology & visual science · 2014Article
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Complement C5a, a potent anaphylatoxin, is a candidate target molecule for the treatment of inflammatory diseases, such as myocardial ischemia/reperfusion injury, RA, and the antiphospholipid syndrome. In contrast, up until now, no specific contribution of C5a and its receptor, C5aR, was recognized in diseases of antibody-dependent type II autoimmunity. Here we identify C5a as a novel key mediator of autoimmune hemolytic anemia (AIHA) and show that mice lacking C5aR are partially resistant to this IgG autoantibody-induced disease model. Upon administration of anti-erythrocyte antibodies, upregulation of activating Fcgamma receptors (FcgammaRs) on Kupffer cells, as observed in WT mice, was absent in C5aR-deficient mice, and FcgammaR-mediated in vivo erythrophagocytosis was impaired. Surprisingly, in mice deficient in FcgammaRI and FcgammaRIII, anti-erythrocyte antibody-induced C5 and C5a production was abolished, demonstrating the existence of a previously unidentified FcgammaR-mediated C5a-generating pathway. These results show that the development of a full-blown antibody-dependent autoimmune disease requires C5a--produced by and acting on FcgammaR--and may suggest therapeutic benefits of C5 and/or C5a/C5aR blockade in AIHA and other diseases closely related to type II autoimmune injury.
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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.