He Visceral Leishmaniasis (VL) is a chronic disease with high mortality rate. According to the Secretary of Epidemiological Surveillance of the state of São Paulo, Araçatuba region has the largest number of cases. The dog is the domestic reservoir of visceral leishmaniasis, with great epidemiological importance in endemic areas. The infected dog can transmit the parasite to humans through the sandfly vector (Lutzomyia longipalpis), with the canine disease usually precede human cases. To survive within mononuclear cells of the host, the leishmania develop escape mechanisms by altering the response of phagocytic cells. The progression of canine infection is accompanied by a failure of cellular immunity with apoptosis of T lymphocytes and production of cytokines which suppress the microbicidal function of macrophages. Evidence suggests that depletion or apoptosis of T lymphocytes is related to the PD-1 receptor expression, a new member of the B7 costimulatory family inhibitory, the surface of these cells. The exhaustion of the establishment is also linked to decreased IL-2 by T cells of the canine visceral leishmaniasis Although the exhaustion of lymphoproliferative response is associated with the PD1 because its lock can restore lymphoproliferation, no studies have evaluated whether IL 2 is engaged with the recovery of the cellular response. Thus, our objective is to block the binding between PD-1 and PD-1L in cell culture of spleen leukocytes in naturally infected dogs and assess whether IL-2 levels are increased and further evaluate the recovery of the cellular response reduces the load parasitic.
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