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Genetic dissection of a major haplotype associated with arthritis reveal FcγR2b and FcγR3 to act additively
Karolinska Institute, Stockholm, Sweden.
Karolinska Institute, Stockholm, Sweden.
University of Southampton Faculty of Medicine, Southampton, United Kingdom.
Karolinska Institute, Stockholm, Sweden; Southern Medical University, Guangzhou, China.ORCID-id: 0000-0001-7790-8197
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2021 (engelsk)Inngår i: European Journal of Immunology, ISSN 0014-2980, E-ISSN 1521-4141, Vol. 51, nr 3, s. 682-693Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

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.

sted, utgiver, år, opplag, sider
2021. Vol. 51, nr 3, s. 682-693
Emneord [en]
Cia9 locus, Fc gamma receptor, FcγR2b, FcγR3, collagen-induced arthritis
HSV kategori
Identifikatorer
URN: urn:nbn:se:hh:diva-48320DOI: 10.1002/eji.202048605PubMedID: 33244759OAI: oai:DiVA.org:hh-48320DiVA, id: diva2:1702426
Tilgjengelig fra: 2022-10-10 Laget: 2022-10-10 Sist oppdatert: 2023-03-08bibliografisk kontrollert

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Nandakumar, Kutty Selva

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