Cutaneous Leishmaniasis: The Complexity of Host’s Effective Immune Response against a Polymorphic Parasitic Disease

Figure 4

Activation of host immunity by cutaneous species of Leishmania. After skin infection, Leishmania promastigotes are uptake by phagocytes. IL-12 is secreted by activated DCs, and parasite antigens are presented by APCs, resulting in lymphocyte activation and secretion of proinflammatory (IL-2, IFN-γ, and TNF-α) cytokines that can activate MΦ microbicide mechanisms, leading to parasite inactivation. When IL-4, IL-5, and IL-13 predominate parasite replicates, allowing disease establishment. Differentiation of Th17 lymphocytes lead to a strong inflammatory environment that could cause tissue damage. Regulatory T cells inhibit lymphocyte activity promoting immune homeostasis and favoring disease progress. CL: cutaneous leishmaniasis; DC: dendritic cells, IFN: interferon; IL: interleukin; MΦ: macrophages; N: neutrophils; NO: nitric oxide; Th: T helper cell; Th0: naïve T cells; TNF: tumor necrosis factor; Treg: regulatory T cells.