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R Signaling in the K/B x N Serum Transfer Model of Arthritis1
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 
-chain of the FcR did not show clinical synovitis after
receiving K/BxN sera, erosive lesions in the bone still developed.
Further analysis demonstrated that FcRII-/- mice
manifested accelerated arthritis whereas the FcRIII-/-
mice had a more slowly progressing arthritis. Paw swelling required
FcR 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 FcRII and FcRIII, and a
subacute component, which results in bone erosion, even in the absence
of FcR signaling.
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