The present study demonstrates that endogenous production of IL-12 is cruci
al for survival in Staphylococcus aureus-induced arthritis in mice. Staphyl
ococcal load is enhanced in several organs, because of lack of IL-12. This
might be due to decreased production of IFN-gamma in IL-12-deficient mice.
Although IL-12-deficient mice were exposed to higher staphylococcal load, t
hey demonstrated no increased severity of arthritis as compared with contro
l animals.