Persistent immune activation in TB/HIV co-infection involved not only enhanced production of proinflammatory (IL-6, IFN-γ, CXCL9, CXCL10, and iNOS) as well as anti-inflammatory (IL-1RA, IL-10, Arg-1, and IDO) mediators but also elevated numbers of myeloid cells with an aberrant phenotype and morphology characteristic of MDSCs in TB-infected lymph nodes. This evidence concerns the gene CXCL10 and tuberculosis.