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International Immunology Advance Access published online on January 13, 2006
International Immunology, doi:10.1093/intimm/dxh380
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© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
Received August 3, 2005
Accepted December 8, 2005

Article

The MHC class I-related FcRn ameliorates murine Lyme arthritis

Helena Crowley 1, Joseph Alroy 2, Thomas J. Sproule 3, Derry Roopenian 3, and Brigitte T. Huber 1 *

1 Department of Pathology, Tufts University School of Medicine, Boston, MA 02111, USA
2 Department of Pathology, Tufts University School of Veterinary Medicine, Grafton, MA 01538, USA
3 Jackson Laboratory, Bar Harbor, ME 04609, USA

* To whom correspondence should be addressed.
Brigitte T. Huber, E-mail: brigitte.huber{at}tufts.edu


  Abstract

The identification of the neonatal FcR (FcRn) as an IgG homeostasis regulator has led to research aimed at delineating a role for FcRn in humorally mediated disease. FcRn is a class I-related molecule that prolongs the half-life of serum IgG by preferentially binding IgG at low pH and inhibiting its degradation. Its role in protective immunity to infectious organisms is unknown. We investigated the function of FcRn in the murine model of Lyme arthritis, caused by infection with Borrelia burgdorferi. We infected FcRn-/- and wild-type mice with B. burgdorferi and monitored the development of arthritis. Infected FcRn-/- mice demonstrated decreased serum levels of anti-B. burgdorferi antibodies and borreliacidal activity. Moreover, these mutant mice developed increased ankle swelling and joint histopathology following infection. Our data suggest that FcRn ameliorates murine Lyme arthritis by preventing the degradation of protective borreliacidal antibodies.

Keywords: bacterial; Borrelia burgdorferi; inflammation; rodent.
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