These data suggest that HIV-TB patients are not able to generate an adequate response for the containment of the bacteria, as a result of the reduction in IFN-γ/IL-10 and IFN-γ/IL-17A ratios and the combined production of pro-inflammatory cytokines (TNF-α and IL-17A) which unrestrained levels are associated with immunopathology [19, 20]. This evidence concerns the gene IL17A and tuberculosis.