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Clinical and Vaccine Immunology, May 2007, p. 510-517, Vol. 14, No. 5
1071-412X/07/$08.00+0     doi:10.1128/CVI.00005-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Anti-p19 Antibody Treatment Exacerbates Lyme Arthritis and Enhances Borreliacidal Activity{triangledown}

Sara Heil Peterson,1,2 Dean T. Nardelli,1,4 Thomas F. Warner,5 Steven M. Callister,6 Jose R. Torrealba,5 and Ronald F. Schell1,2,3,4*

Wisconsin State Laboratory of Hygiene,1 Departments of Bacteriology,2 Medical Microbiology and Immunology,3 Pathobiological Sciences, University of Wisconsin,4 Department of Pathology, Veterans Administration Hospital, Madison, Wisconsin,5 Microbiology Research Laboratory and Section of Infectious Diseases, Gundersen Lutheran Medical Center, La Crosse, Wisconsin6

Received 3 January 2007/ Returned for modification 22 February 2007/ Accepted 1 March 2007

Considerable effort has been made to elucidate the mechanism of Lyme arthritis. We focused on p19, a cell cycle-regulating molecule, because it is known to inhibit cell cycle division of T lymphocytes which may be responsible for the induction of arthritis. We show that anti-p19 antibody treatment enhances the inflammatory response normally detected at the tibiotarsal joints of Borrelia burgdorferi-vaccinated and Borrelia bissettii-challenged mice. Specifically, anti-p19 antibody treatment augmented the severity of inflammation within the synovial and subsynovial tissue. Moreover, treatment with anti-p19 antibody caused severe erosion of cartilage and bone with ankle joint destruction. In addition, anti-p19 antibody treatment of Borrelia-vaccinated and -challenged mice enhanced the borreliacidal antibody response, especially against the vaccine isolate. The novel activities of anti-p19 antibody show that p19 may be an important therapeutic site for the treatment of Lyme arthritis.

* Corresponding author. Mailing address: University of Wisconsin, Wisconsin State Laboratory of Hygiene, 465 Henry Mall, Madison, WI 53706. Phone: (608) 262-3634. Fax: (608) 265-3451. E-mail: RFSchell{at}wisc.edu

{triangledown} Published ahead of print on 14 March 2007.

Clinical and Vaccine Immunology, May 2007, p. 510-517, Vol. 14, No. 5
1071-412X/07/$08.00+0     doi:10.1128/CVI.00005-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Brentano, F, Ospelt, C, Stanczyk, J, Gay, R E, Gay, S, Kyburz, D (2009). Abundant expression of the interleukin (IL)23 subunit p19, but low levels of bioactive IL23 in the rheumatoid synovium: differential expression and Toll-like receptor-(TLR) dependent regulation of the IL23 subunits, p19 and p40, in rheumatoid arthritis. Ann Rheum Dis 68: 143-150 [Abstract] [Full Text]  
  • Nardelli, D. T., Callister, S. M., Schell, R. F. (2008). Lyme Arthritis: Current Concepts and a Change in Paradigm. CVI 15: 21-34 [Full Text]  


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