Migration of immune cells is orchestrated by a fine balance of cytokine and chemokine responses. During Leishmania macrophage interaction, either pro inflammatory or anti-inflammatory cytokines are produced, having an impact in the establishment of infection and further clinical outcome (Navas et al. 2014). Toll like receptors, GPCRs such as the purinergic receptors P2YRs, complement receptor 3A and interleukin receptor 15 amongst others, have been associated with the production of pro inflammatory cytokines (Lai and Gallo 2012 & Cekic et al. 2016). A strong pro inflammatory response in the acute phase of the infection helps to control the parasite load when the recruited cells enhance microbiocidal mechanisms. However, alterations in the chemokine network may contribute to uncontrolled immune responses that can modulate parasite survival and promote or mitigate the associated immunopathology, thereby influencing the outcome of infection (Navas et al. 2014).