Borrelia burgdorferi–Infected, Interleukin-6–Deficient Mice

Summary: Recently, interleukin (IL)-6 was shown to be one of the earliest factors that trigger the differentiation of naive T cells into effector Th2 cells in vitro. Lyme arthritis was studied in IL-6–deficient mice, since joint inflammation is influenced by the T helper cell response against Borrelia burgdorferi. Arthritis incidence increased in B. burgdorferi–infected IL-6– deficient mice compared with that in controls. Furthermore, splenocytes of B. burgdor- feri–infected IL-6–deficient mice produced significantly less IL-4 in response to Borrelia an- tigens than did C57BL/6 (B6) mice, and B. burgdorferi–specific IgG2b levels were significantly reduced in IL-6–deficient mice at 60 days of infection. These results extend previous in vitro observations by demonstrating an in vivo role for IL-6 in the differentiation of CD4 T cells toward a Th2 phenotype and further show that CD4 T cell responses influence murine Lyme arthritis.