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The Journal of Immunology, 2002, 169: 6604-6609.
Copyright © 2002 by The American Association of Immunologists

The Role of Fc{gamma}R Signaling in the K/B x N Serum Transfer Model of Arthritis1

Maripat Corr2 and Brian Crain

Division of Rheumatology, Allergy, and Immunology and Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla, CA 92093

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 Fc{gamma}R did not show clinical synovitis after receiving K/BxN sera, erosive lesions in the bone still developed. Further analysis demonstrated that Fc{gamma}RII-/- mice manifested accelerated arthritis whereas the Fc{gamma}RIII-/- mice had a more slowly progressing arthritis. Paw swelling required Fc{gamma}R 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 Fc{gamma}RII and Fc{gamma}RIII, and a subacute component, which results in bone erosion, even in the absence of Fc{gamma}R signaling.




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