LAUSR

&NA; The immune mechanisms responsible for development of Lyme arthritis are partially understood with interleukin‐17 (IL‐17) and gamma‐interferon (IFN‐&ggr;) playing a generally accepted role. Elevated levels of IL‐17 and/or IFN‐&ggr; have been reported in samples from human Lyme arthritis patients and experimental mice. In addition, IL‐17 and IFN‐&ggr; have been implicated in the onset of arthritis in Borrelia‐primed and ‐infected C57BL/6 mice. Recently, we showed that IL‐17‐deficient mice developed swelling and histopathological changes consistent with arthritis in the presence of high levels of IFN‐&ggr;. We hypothesized that neutralization of IFN‐&ggr; in IL‐17‐deficient mice would inhibit Borrelia‐induced arthritis. Our results, however, showed that swelling of the hind paws and histopathological changes of arthritis did not differ between Borrelia‐primed and ‐infected IL‐17‐deficient and wild‐type mice with or without neutralization of IFN‐&ggr;. We also found higher levels of tumor necrosis factor alpha (TNF‐&agr;) and IL‐6 in the popliteal lymph node cells of Borrelia‐primed and ‐infected IL‐17‐deficient mice after neutralization of IFN‐&ggr;. These results suggest that multiple cytokines interact in the development of Borrelia‐induced arthritis.