Interleukin-23 is required for development of arthritis in mice vaccinated and challenged with Borrelia species

Nicholas J. Kotloski, Dean T. Nardelli, Sara Heil Peterson, Jose R. Torrealba, Thomas F. Warner, Steven M. Callister, Ronald F. Schell

Research output: Contribution to journalArticle

33 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1199-1207
Number of pages9
JournalClinical and Vaccine Immunology
Issue number8
Publication statusPublished - Aug 2008


ASJC Scopus subject areas

  • Clinical Biochemistry
  • Immunology
  • Immunology and Allergy
  • Microbiology (medical)

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