Abstract
Abstract Human regulatory T cells can be generated through a number of known pathways in vivo and in vitro. Simultaneous engagement of the TCR and complement regulator CD46 on human CD4+ T cells induces adaptive Treg development. These CD46-induced Treg, also known as 'complement-induced Treg' or 'cTreg,' have been shown to suppress bystander CD4+ T cells activated in vitro with crosslinking antibodies to CD3 and CD28. Here we offer the first description of cTreg suppression of human effector T cells in an APC-dependent system of pathogen infection. We found that soluble molecules secreted by cTreg suppress Mycobacterium tuberculosis-specific CD4+, CD8+, and γδ T cell responses. These immunosuppressive effects were mediated in part by IL-10 and in part by other as yet unidentified soluble factors acting synergistically with IL-10. In addition, our results indicate that different mechanisms may be involved in the suppression of αβ and γδ T cells. We further show that APC functions were not affected by cTreg, indicating direct suppression of pathogen-specific T cells. Modulating the immunosuppressive functions of this Treg subset could lead to improved tuberculosis therapeutics or vaccines.
Published Version
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