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We report that stimulation of Mycobacterium tuberculosis (M. tuberculosis) secretory antigen (MTSA)-differentiated dendritic cells (DCs) and MTSA-matured DCs with M. tuberculosis cell extract (CE) down-regulated proinflammatory responses to CE-primed T (CE-T) cells by increasing surface expression of CD86 after CE stimulation. CE stimulation also decreased interleukin (IL)-12p40 and interferon (IFN)- gamma levels and increased IL-10 and transforming growth factor- beta 1 (TGF- beta 1) levels from these DCs. Blocking either CD86, IL-10, or TGF- beta with monoclonal antibodies before CE stimulation restored the attenuated T helper 1 (Th1) responses of CE-T cells. Conversely, treatment of these DCs with IL-12p70 and/or IFN- gamma completely restored Th1 responses from CE-T cells. These results indicate that M. tuberculosis secretory antigens down-regulate proinflammatory Th1 responses to mycobacteria by differentially modulating the cytokine profiles and surface densities of costimulatory molecules on DCs. Of importance, this down-regulation is independent of the maturation status of MTSA-activated DCs and can be rescued after treatment of DCs with IFN- gamma or IL-12.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Dominance of CD86, Transforming Growth Factor–β1, and Interleukin‐10 in<i>Mycobacterium tuberculosis</i>Secretory Antigen–Activated Dendritic Cells Regulates T Helper 1 Responses to Mycobacterial Antigens

Dominance of CD86, Transforming Growth Factor–β1, and Interleukin‐10 inMycobacterium tuberculosisSecretory Antigen–Activated Dendritic Cells Regulates T Helper 1 Responses to Mycobacterial Antigens