To investigate the role of B cells in experimental, superantigen-mediated S
taphylococcus aureus arthritis and sepsis, me used gene-targeted B-cell-def
icient mice. The mice were inoculated intravenously with a toxic shock synd
rome toxin 1 (TSST-1)-producing S. aureus strain. The B-cell-deficient and
thus agamma-globulinemic mice showed striking similarities to the wild-type
control animals with respect to the development of arthritis, the mortalit
y rate, and the rate of bacterial clearance. Surprisingly, we found that th
e levels of gamma interferon in serum were significantly lower (P < 0.0001)
in B-cell-deficient mice than in the controls, possibly due to impaired su
perantigen presentation and a diminished expression of costimulatory molecu
les. In contrast, the levels of interleukin-4 (IL-4), IL-6, and IL-10 in se
rum were equal in both groups. Our findings demonstrate that neither mature
B cells nor their products significantly contribute to the course of S. au
reus-induced septic arthritis.