“…Evidence suggests that several factors may affect this process during leishmanial infection: (i) the cytokine environment present during the initial events of cell differentiation; (ii) the interaction with regional antigenpresenting cells, which can preferentially present different classes of antigens; (iii) the influence of other costimulatory signals; and (iv) the differential signalling mechanisms used by the TH cell subsets after the engagement of the T-cell receptor (3,85,171,205,207). Evidence of cross-regulation of TH cell subsets also exists (205), but it is still unclear how or to what extent the protective and the disease-promoting T-cell subpopulations interact during leishmanial infection (118,124,125,166,171,270,271). Contributions by other lymphocyte populations, such as CD8+ (83,122,270,292,299) and gamma-delta T cells (200), to the mediation of protective immunity against leishmanial infection have been shown but are less well understood.…”