CD4+ T-cell–independent mechanisms suppress reactivation of latent tuberculosis in a macaque model of HIV coinfection

摘要: The synergy between Mycobacterium tuberculosis (Mtb) and HIV in coinfected patients has profoundly impacted global mortality because of (TB) AIDS. significantly increases rates reactivation latent TB infection (LTBI) to active disease, with the decline CD4(+) T cells believed be major causality. In this study, nonhuman primates were Mtb simian immunodeficiency virus (SIV), recapitulating human coinfection. A majority animals exhibited rapid replication, progressing disseminated increased SIV-associated pathology. Although a severe loss pulmonary was observed all macaques, subpopulation still able prevent maintain LTBI. Investigation immune responses pathology cohort demonstrated that CD8(+) memory T-cell proliferation, higher granzyme B production, expanded B-cell follicles correlated protection from reactivation. Our findings reveal mechanisms control SIV- TB-associated These CD4-independent protective warrant further studies humans their infection. Moreover, these will provide insight into natural immunity guide development novel vaccine strategies immunotherapies.