ArticleThe Journal of clinical investigation2002
C5a anaphylatoxin is a major regulator of activating versus inhibitory FcgammaRs in immune complex-induced lung disease.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed, 283 citations in OpenAlex.
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- There Is Strength in Numbers: Quantitation of Fc Gamma Receptors on Murine Tissue-Resident Macrophages.International journal of molecular sciences · 2021Article
- Complement Activation in the Treatment of B-Cell Malignancies.Antibodies (Basel, Switzerland) · 2020Review
- Glycosylation-dependent opsonophagocytic activity of staphylococcal protein A antibodies.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Mechanistic inferences from clinical reports of SARS-CoV-2.Infectious diseases (London, England) · 2020Review
- Anti-Citrullinated Protein Antibodies in Patients with Rheumatoid Arthritis: Biological Effects and Mechanisms of Immunopathogenesis.International journal of molecular sciences · 2020Review
- An intranasally administered monoclonal antibody cocktail abrogates ricin toxin-induced pulmonary tissue damage and inflammation.Human vaccines & immunotherapeutics · 2020Article
- Complement System: a Neglected Pathway in Immunotherapy.Clinical reviews in allergy & immunology · 2020Review
- Immunotherapy in Multiple Myeloma.Cells · 2020Review
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- Fc Gamma Receptors and Complement Component 3 Facilitate Anti-fVIII Antibody Formation.Frontiers in immunology · 2020Article
60 more citing papers are in PubMed but not listed here.
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IgG Fc receptors (FcgammaRs, especially FcgammaRIII) and complement (in particular, C5a anaphylatoxin) are critical effectors of the acute inflammatory response to immune complexes (ICs). However, it is unknown whether and how these two key components can interact with each other in vivo. We use here a mouse model of the acute pulmonary IC hypersensitivity reaction to analyze their potential interaction. FcgammaRIII and C5aR are coexpressed on alveolar macrophages (AMs), and both FcgammaRIII and C5aR mutant mice display impaired immune responses. We find that recombinant human C5a (rhC5a) can control inverse expression of various FcgammaRs, and costimulation of ICs with rhC5a results in strong enhancement of FcgammaRIII-triggered cellular activation in vitro and in vivo. Moreover, we show here that early IC-induced bioactive C5a, and its interaction with C5aR, causes induction of activating FcgammaRIII and suppression of inhibitory FcgammaRII on AMs that appears crucial for efficient cytokine production and neutrophil recruitment in lung pathology. Therefore, C5a, which is a potent chemoattractant, has a broader critical function in regulating the inhibitory/activating FcgammaRII/III receptor pair to connect complement and FcgammaR effector pathways in immune inflammation.
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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.