| First Author | Corr M | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 11 | Pages | 6604-9 |
| PubMed ID | 12444173 | Mgi Jnum | J:124384 |
| Mgi Id | MGI:3721456 | Doi | 10.4049/jimmunol.169.11.6604 |
| Citation | Corr M, et al. (2002) The role of FcgammaR signaling in the K/B x N serum transfer model of arthritis. J Immunol 169(11):6604-9 |
| abstractText | Spontaneous arthritis in the KRN transgenic mouse (K/BxN) model is due to the autoreactivity of the transgenic TCR and subsequent induction of autoantibodies directed against glucose-6-phosphate isomerase. These autoantibodies transfer clinically apparent arthritis into most recipient mouse strains and systemic catabolism of the transferred Abs attenuates paw swelling. Although mice deficient in the common gamma-chain of the FcgammaR did not show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still developed. Further analysis demonstrated that FcgammaRII(-/-) mice manifested accelerated arthritis whereas the FcgammaRIII(-/-) mice had a more slowly progressing arthritis. Paw swelling required FcgammaR expression by bone marrow-derived cells and mast cells substantially contributed to the acute phase of paw swelling. In the K/BxN serum transfer model of arthritis, there is a clinically apparent acute phase, which is modulated by FcgammaRII and FcgammaRIII, and a subacute component, which results in bone erosion, even in the absence of FcgammaR signaling. |
