BALB / c and anti‐IL‐12‐treated C3H mice infected with Leishmania major develop a Th2 cell response. However, in contrast to BALB / c mice, C3H mice treated transiently with an anti‐IL‐12 monoclonal antibody switch from a Th2 to a Th1 response and resolve their lesions once treatment is terminated. We report here that the critical difference in the Th2 response between BALB / c and C3H mice is in their ability to respond to IL‐12. Thus, C3H mice with a Th2 response maintain a CD4⁺ T cell population that expresses IL‐12 receptor β1 and β2 mRNA and produces IFN‐γ after exposure to IL‐12. These results indicate that Th2 cell populations from different genetic backgrounds differ in their stability, and that this difference can be related to differential regulation of the IL‐12 receptor.