The role of FcγR signaling in the K/B× N serum transfer model of arthritis

M Corr, B Crain - The Journal of Immunology, 2002 - journals.aai.org
M Corr, B Crain
The Journal of Immunology, 2002journals.aai.org
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 γ-chain of the FcγR did not
show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still …
Abstract
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 γ-chain of the FcγR did not show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still developed. Further analysis demonstrated that FcγRII−/− mice manifested accelerated arthritis whereas the FcγRIII−/− mice had a more slowly progressing arthritis. Paw swelling required FcγR 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 FcγRII and FcγRIII, and a subacute component, which results in bone erosion, even in the absence of FcγR signaling.
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