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English: Impact of Leishmania infection on immune cells. Leishmania spp. interacts with multiple innate immune cells modulating their phenotype and function, as well as the adaptive immune responses. Mast cells collaborate in disease progression by secreting IL-4 and IL-13 fostering Th2 responses and parasite survival (panel 1). Neutrophils, macrophages, and DCs can either eliminate or promote parasite survival. Recruited neutrophils eliminate leishmanial parasites through phagocytosis, ROS, and NETs release. Leishmania can survive transiently within neutrophils by inhibiting phagolysosome biogenesis and oxidative stress, and by delaying neutrophil apoptosis. Infected neutrophils also secrete IL-8 and MIP1β, which attract additional neutrophils and other phagocytic cells, favoring Leishmania survival and pathology (panel 2). Macrophages can be differentiated in M1 or M2 during leishmaniasis. M1 macrophages produce proinflammatory cytokine and chemokines, NO and ROS, booster Th1 responses, and favor disease control. M2 macrophages increase the production of IL-10 and TGFβ, and support Th2 response and disease progression (panel 3). DCs regulate immune responses against Leishmania by migrating to the draining lymph nodes to present Leishmania-derived antigen to naïve T cells. DCs can induce the differentiation of Th1 by secreting IL-12 and IL-27 or Th2, by blocking IL-12 secretion (panel 4). NK cells have a protective role in leishmaniasis by secreting IFNγ to boost Th1 response (panel 5). IL; interleukin IFNγ; ROS; reactive oxidative species, NO; nitric oxide, NETs; neutrophil extracellular traps, MIP; macrophage; inflammatory protein, TNFα; tumor necrosis factor α, TGFβ; transforming growth factor-β, NK; natural killer.