CCR5 and cutaneous leishmaniasis: As CCR5 controls thymic egress of Tregs during infection39 and it has been showed that during cutaneous leishmaniasis CCR5-dependent homing of Tregs regulates the proinflammatory response and favor pathogen persistence40, it is plausible to suggest that increase in CCR5 expression could induce increased migration (egress from thymus) to inflammatory sites, favoring parasite persistence in secondary lymphoid organs such as spleen.