Interleukin 17 (IL‐17) plays a critical role in inflammation and autoimmunity. Very little is known about IL‐17 in protozoa infection. Here, we show

Cutaneous leishmaniasis (CL) caused byLeishmania braziliensisis characterized by a strong Th1 response that leads to skin lesion development. In areas whereL. braziliensistransmission is endemic, up to 15% of healthy subjects have tested positive for delayed-type hypersensitivity to soluble leishmania antigen (SLA) and are considered to have subclinical (SC) infection. SC subjects produce less gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α) than do CL patients, but they are able to control the infection. The aim of this study was to characterized the role of CD8⁺T cells in SC infection and in CL. Peripheral blood mononuclear cells (PBMC) were stimulated with SLA to determine the frequencies of CD4⁺IFN-γ⁺and CD8⁺IFN-γ⁺T cells. Monocytes from PBMC were infected withL. braziliensisand cocultured with CD8⁺T cells, and the frequencies of infected monocytes and levels of cytotoxicity markers, target cell apoptosis, and granzyme B were determined. The frequency of CD8⁺IFN-γ⁺cells after SLA stimulation was higher for SC individuals than for CL patients. The frequency of infected monocytes in SC cells was lower than that in CL cells. CL CD8⁺T cells induced more apoptosis of infected monocytes than did SC CD8⁺T cells. Granzyme B production in CD8⁺T cells was higher in CL than in SC cells. While the use of a granzyme B inhibitor decreased the number of apoptotic cells in the CL group, the use of z-VAD-FMK had no effect on the frequency of these cells. These results suggest that CL CD8⁺T cells are more cytotoxic and may be involved in pathology.