Although non-specific IP10 increases have been described in acute and chronic diseases other than TB [34], [35], [36], [37], these findings suggest that IP10 expression may vary during the course of disease progression, maybe with higher expression during the primary stages of granuloma formation, which involves the recruitment of monocytes and Th1 gammadelta T-cells [38] and lower expression in the presence of progressive unchecked infections, in the presence of immunosuppression, as described for INFγ. This evidence concerns the gene CXCL10 and tuberculosis.