These data corroborate our earlier findings, where we showed that chimeras lacking B cell-derived IL-4 had a skewed Th1 response characterized by up-regulation of the Th1 cytokine IFN-γ and down-regulation of the Th2 cytokines IL-4 and IL-13, that consequently rendered these mice resistant to L. major induced cutaneous leishmaniasis (9). The gene discussed is IFNG; the disease is cutaneous leishmaniasis.