| First Author | Vaartjes D | Year | 2021 |
| Journal | Eur J Immunol | Volume | 51 |
| Issue | 3 | Pages | 682-693 |
| PubMed ID | 33244759 | Mgi Jnum | J:304444 |
| Mgi Id | MGI:6508636 | Doi | 10.1002/eji.202048605 |
| Citation | Vaartjes D, et al. (2021) Genetic dissection of a major haplotype associated with arthritis reveal FcgammaR2b and FcgammaR3 to act additively. Eur J Immunol 51(3):682-693 |
| abstractText | A haplotype with tightly linked Fc gamma receptor (FcgammaR) 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 FcgammaR gene cluster and a recombination between the FcgammaR2b and FcgammaR3 loci gave us the opportunity to separately study their impact. We identified the NOD-derived FcgammaR2b and FcgammaR3 alleles as disease-promoting for arthritis development without impact on antibody secretion. We further found that macrophage-mediated phagocytosis was directly correlated to FcgammaR3 expression in the congenic mice. In conclusion, we positioned FcgammaR2b and FcgammaR3 alleles as disease regulatory and showed that their genetic polymorphisms independently and additively control innate immune cell activation and arthritis. |
