The Journal of Experimental Medicine
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Published online 13 February 2006 doi:10.1084/jem.20051951
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 2, 275-280
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BRIEF DEFINITIVE REPORT

 Human antibodies induce arthritis in mice deficient in the low-affinity inhibitory IgG receptor Fc{gamma}RIIB

Stefka B. Petkova1, Konstantin N. Konstantinov2, Thomas J. Sproule1, Bonnie L. Lyons1, Moheeb Al Awwami1, and Derry C. Roopenian1

1 The Jackson Laboratory, Bar Harbor, ME 04605
2 Department of Internal Medicine, Division of Rheumatology, The University of New Mexico, Albuquerque, NM 87122

CORRESPONDENCE Derry C. Roopenian: dcr{at}jax.org

Rheumatoid arthritis (RA) is a complex autoimmune disease with a poorly understood pathogenesis. The disease is associated with polyclonal B cell activation and the production of autoantibodies (autoAbs), but there is a longstanding controversy as to whether such Abs contribute to, or are secondary to, the pathogenesis of RA. To address the potential pathogenicity of human RA–associated Abs, we developed a passive transfer model involving mice deficient in the low-affinity inhibitory Fc receptor, Fc{gamma}RIIB. We report that plasma or serum from patients with active RA can induce inflammation and histological lesions in Fc{gamma}RIIB–/– mice consistent with arthritis, and that this pathogenic activity is caused by the immunoglobulin G–rich fraction. Our results suggest that humoral autoimmunity can contribute directly to autoimmune arthritis, and that Fc{gamma}RIIB–/– mice are a promising model to evaluate the arthritogenic potential of human autoAbs.


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