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Clin. Vaccine Immunol. doi:10.1128/CVI.00129-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Interleukin (IL)-23 is Required for the Development of Arthritis in Borrelia-Vaccinated and -Challenged Mice

Wisconsin State Laboratory of Hygiene, and Departments of Bacteriology, Medical Microbiology and Immunology, Pathobiological Sciences, and Pathology and Laboratory Medicine, University of Wisconsin, Madison, Wisconsin; Microbiology Research Laboratory and Section of Infectious Diseases, Gundersen Lutheran Medical Center, La Crosse, Wisconsin

^* To whom correspondence should be addressed. Email: rfschell{at}wisc.edu.

	Abstract

We recently hypothesized that T helper (Th)-17 cells and their associated cytokines are involved in the development of arthritis following infection with Borrelia burgdorferi. Here, we show that interleukin (IL)-23, a survival factor for Th17 cells, is required for the induction of arthritis in Borrelia burgdorferi strain 297-vaccinated and B. bissettii-challenged mice. When Borrelia-vaccinated and -challenged mice were administered antibodies to the p19 subunit of IL-23, they failed to develop the histopathologic changes observed in untreated vaccinated and challenged mice. In addition, viable B. bissettii organisms stimulated 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 and Borrelia-immune lymph node cells, 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.