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Clinical and Vaccine Immunology, August 2008, p. 1199-1207, Vol. 15, No. 8
1071-412X/08/$08.00+0     doi:10.1128/CVI.00129-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Interleukin-23 Is Required for Development of Arthritis in Mice Vaccinated and Challenged with Borrelia Species{triangledown}

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

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

Received 11 April 2008/ Returned for modification 9 June 2008/ Accepted 13 June 2008

We recently hypothesized that T helper 17 (Th17) cells and their associated cytokines are involved in the development of arthritis following infection with Borrelia burgdorferi. Here, we show that interleukin-23 (IL-23), a survival factor for Th17 cells, is required for the induction of arthritis in mice vaccinated with B. burgdorferi strain 297 and challenged with "Borrelia bissettii." When Borrelia-vaccinated and -challenged mice were given antibodies to the p19 subunit of IL-23, they failed to develop the histopathological changes observed in untreated vaccinated and challenged mice. In addition, viable B. bissettii organisms stimulated the secretion of IL-17 from Borrelia-immune lymph node cells during in vitro culture. When anti-IL-23 p19 antibody was included in cultures of B. bissettii organisms and Borrelia-immune lymph node cells, the production of IL-17 was reduced to levels observed in cultures containing immune cells alone. Taken together, these results support the hypothesis that Th17 cell-associated cytokines are involved in the development of Borrelia-mediated arthritis. These findings provide insight into previously overlooked immune mechanisms responsible for the development 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 25 June 2008.

Clinical and Vaccine Immunology, August 2008, p. 1199-1207, Vol. 15, No. 8
1071-412X/08/$08.00+0     doi:10.1128/CVI.00129-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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