Biopsies from human localized cutaneous lesions (LCL n = 7) or disseminated lesions (DL n = 8) cases were characterized according to cellular infiltration, frequency of cytokine (IFN-γ, TNF-α) Cutaneous leishmaniasis is a worldwide disease with severe deformating potential in new world. It affects preferentially young economically active patients representing a large burden to the public health system in developing countries. Protection against all forms of leishmaniasis is dependent on cell-mediated immunity (CMI), but the contribution of some cells and cytokines in human disease deserves further scrutiny.CD8 + T cells have been implicated in protection (Muller et al. 1991) being high IFN-γ producers in a murine model of leishmaniasis (Chan 1993). Their role seems to be more in the secondary than in the primary immune response (Muller et al. 1993(Muller et al. , 1994. On the other hand, the course of leishmaniasis in mice lacking beta 2-microglobulin (beta 2-m) gene did not differ from their wild-type counterparts (Overath & Harbecke 1993, Wang et al. 1993, Huber et al. 1998) lessening a role of antigen presentation by major histocompatibility complex class I (MHC I) molecules. In man, a higher percentage of CD8 + over CD4 + T cells was found in mucocutaneous leishmaniasis (MCL) lesions (Castes & Tapia 1998), compared to localized cutaneous lesions (LCL), although similar distributions of CD4 + and CD8 + in LCL have been reported (Barral et al. 1987, Esterre et al. 1992, Lima et al. 1994. The presence of cytotoxic CD8 + T cells has been reported in peripheral blood of MCL but not in LCL patients (Brodskyn et al. 1997). Expansion of CD8 + T cells occurs in the peripheral blood of individuals vaccinated against leishmaniasis (Mendonça et al. 1995, Gurunathan et al. 2000. Especially, the percentage of activated CD8 + T cells was higher in fast responding than in slow responding volunteers to vaccination (Pompeu et al. 2001).The role of B cells in leishmaniasis is also not clear. High antibody levels are present in the more severe clinical form of the cutaneous disease, namely diffuse cutaneous leishmaniasis (DCL) (Schurr et al. 1986, Mengistu et al. 1990), but B cell depletion does not alter the susceptibility or resistance pattern to Leishmania infection in mice (Babai et al. 1999, Brown & Reiner 1999. It seems that B cells are important to induce anti-Leishmania CD4 + Th1 cells and DTH reaction, in the resistant mouse strain, and take part in the humoral response development in susceptible animals (Scott & Farrell 1982, Scott et al. 1986).Predominance of Th1 cytokines like IFN-γ, IL-12, IL-2 and TNF-α over Th2 cytokines, IL-4, IL-5 IL-10 and TGF-β, is correlated in mice to the resistance profile against Leishmania infection (Belosevic et al. 1989, Chatelain et al. 1992, Lezama-Davila et al. 1992, Barral et al. 1993. Imunological studies in humans demonstrated a combination of Th1 and Th2 cytokines with predominance of Th1 in MCL, Th2 predominate in DCL and predominance of Th1 profile in LCL patients , Castes et...

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