The majority of individuals infected with Leishmania do not develop leishmaniasis and early events in Leishmania infection play a  pivotal role in determine disease expression. In experimental models, neutrophils rapidly infiltrate infected sites and have been associated with both susceptibility and host-protective responses. Macrophages serve as host cells for parasite replication but participate of Leishmania killing process. Activation of NK cells and IL-17 production are observed and they may be involved in parasite killing, as well as tissue damage. While an absence of a type 1 immune response is associated with parasite dissemination, in tegumentary leishmaniasis pathology is dependent of an exacerbated T cell response. In this review the early events in leishmaniasis and the evasion mechanisms used by Leishmania will be discussed, as well as how innate and adaptive immune response may control or mediate pathology in Leishmania infection.