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International Immunology Advance Access originally published online on January 13, 2006
International Immunology 2006 18(3):409-414; 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

The MHC class I-related FcRn ameliorates murine Lyme arthritis

Helena Crowley1, Joseph Alroy2, Thomas J. Sproule3, Derry Roopenian3 and Brigitte T. Huber1

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

Correspondence to: B. T. Huber; E-mail: brigitte.huber{at}tufts.edu

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

Transmitting editor: R. S. Geha


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