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HIV coinfection is the greatest risk factor for transition of latent Mycobacterium tuberculosis infection into active tuberculosis (TB). Epidemiological data reveal both the reduction and the impairment of M. tuberculosis -specific CD4 T cells, although the cellular link and actual mechanisms resulting in immune impairment/suppression need further characterization. M. tuberculosis -specific CD4 T cells play a central role in development of protective immunity against TB, in which they participate in the activation of macrophages through the dendritic cell (DC)-T cell axis. Using an in vitro priming system for generating Ag-specific T cells, we explored if HIV- M. tuberculosis -infected (coinfected) human DCs can dysregulate the M. tuberculosis -specific CD4 T cell phenotype and functionality and subsequently mediate the failure to control M. tuberculosis infection in macrophages. After coculture with coinfected DCs, M. tuberculosis Ag-specific CD4 T cells lost their ability to enhance control of M. tuberculosis infection in infected macrophages. Coinfection of DCs reduced proliferation of M. tuberculosis Ag-specific CD4 T cells without affecting their viability, led to increased expression of coinhibitory factors CTLA-4, PD-1, and Blimp-1, and decreased expression of costimulatory molecules CD40L, CD28, and ICOS on the T cells. Expression of the regulatory T cell markers FOXP3 and CD25, together with the immunosuppressive cytokines TGF-β and IL-10, was also significantly increased by coinfection compared with M. tuberculosis single infection. Our data suggest a pattern in which HIV, through its effect on DCs, impairs the ability of M. tuberculosis -specific CD4 T cells to maintain a latent TB within human macrophages, which could play an early role in the subsequent development of TB.

the journal of immunology/the journal of immunology

HIV Interferes with the Dendritic Cell–T Cell Axis of Macrophage Activation by Shifting <i>Mycobacterium tuberculosis</i>–Specific CD4 T Cells into a Dysfunctional Phenotype

HIV Interferes with the Dendritic Cell–T Cell Axis of Macrophage Activation by Shifting Mycobacterium tuberculosis–Specific CD4 T Cells into a Dysfunctional Phenotype