Amastigote uptake by DCs at the site of infection results in the upregulation of IL-12,[17] which is essential for parasite elimination, and for the effector functions of macrophages.[18] The ability of DCs to present antigens through the MHC I and II pathways leads to stimulation of Leishmania -specific CD4+ and CD8+ T cell responses[19] and is essential for acquired resistance against Leishmania. CD4+ T cells play an important role in antileishmanial immunity and disease outcome. This evidence concerns the gene CD4 and infection.