ArticleEuropean journal of immunology2021
Genetic dissection of a major haplotype associated with arthritis reveal FcγR2b and FcγR3 to act additively.
Article in European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Protective and Pathogenic Antibodies to Citrullinated Antigens.Immunological reviews · 2026Review
- Human MHC Class II and Invariant Chain Knock-in Mice Mimic Rheumatoid Arthritis with Allele Restriction in Immune Response and Arthritis Association.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A subset of type-II collagen-binding antibodies prevents experimental arthritis by inhibiting FCGR3 signaling in neutrophils.Nature communications · 2023Article
- A subset of antibodies targeting citrullinated proteins confers protection from rheumatoid arthritis.Nature communications · 2023Article
- Two major genes associated with autoimmune arthritis, Ncf1 and Fcgr2b, additively protect mice by strengthening T cell tolerance.Cellular and molecular life sciences : CMLS · 2022Article
- Antibodies to Cartilage Oligomeric Matrix Protein Are Pathogenic in Mice and May Be Clinically Relevant in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- Standardization of Antigen-Emulsion Preparations for the Induction of Autoimmune Disease Models.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
A haplotype with tightly linked Fc gamma receptor (FcγR) genes is known as a major locus controlling immune responses and autoimmune diseases, including arthritis. Here, we split a congenic fragment derived from the NOD mouse (Cia9) to study its effect on immune response and arthritis in mice. We found that arthritis susceptibility was indeed controlled by the FcγR gene cluster and a recombination between the FcγR2b and FcγR3 loci gave us the opportunity to separately study their impact. We identified the NOD-derived FcγR2b and FcγR3 alleles as disease-promoting for arthritis development without impact on antibody secretion. We further found that macrophage-mediated phagocytosis was directly correlated to FcγR3 expression in the congenic mice. In conclusion, we positioned FcγR2b and FcγR3 alleles as disease regulatory and showed that their genetic polymorphisms independently and additively control innate immune cell activation and arthritis.
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Registered trials
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