Fundação de Amparo a Pesquisa do Estado da Bahia (FAPESB) (JCB0047/2013 to DP and 5760/2015 to VMB); The Research Foundation Flanders-FWO (G0D6817N to JVW). FC was supported by a grant from the National Institutes of Health (NIH) AI119030. NL received funding from CAPES – Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Grants 88887.142000/2017-00 and 88887.137958/2017-00). VMB and AB are senior investigators of CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico).Leishmania braziliensis infection causes skin ulcers, typically found in localized cutaneous leishmaniasis (LCL). This tissue pathology associates with different modalities of cell necrosis, which are subverted by the parasite as a survival strategy. Herein we examined the participation of necroptosis, a specific form of programmed necrosis, in LCL lesions and found reduced RIPK3 and PGAM5 gene expression compared to normal skin. Assays using infected macrophages demonstrated that the parasite deactivates both RIPK3 and MLKL expression and that these molecules are important to control the intracellular L. braziliensis replication. Thus, LCL-related necroptosis may be targeted to control infection and disease immunopathology.