Central memory Vγ9Vδ2 T lymphocytes primed and expanded by bacillus Calmette-Guérin-infected dendritic cells kill mycobacterial-infected monocytes

In humans, innate immune recognition of mycobacteria, including Mycobacterium tuberculosis and bacillus Calmette-Guérin (BCG), is a feature of cells as dendritic cells (DC) and γδ T cells. In this study, we show that BCG infection of human monocyte-derived DC induces a rapid activation of Vγ9Vδ2 T cells (the major subset of γδ T cell pool in human peripheral blood). Indeed, in the presence of BCG-infected DC, Vγ9Vδ2 T cells increase both their expression of CD69 and CD25 and the production of TNF-α and IFN-γ, in contrast to DC treated with Vγ9Vδ2 T cell-specific Ags. Without further exogenous stimuli, BCG-infected DC expand a functionally cytotoxic central memory Vγ9Vδ2 T cell population. This subset does not display lymph node homing receptors, but express a high amount of perforin. They are highly efficient in the killing of mycobacterial-infected primary monocytes or human monocytic THP-1 cells preserving the viability of cocultured, infected DC. This study provides further evidences about the complex relationship between important players of innate immunity and suggests an immunoregulatory role of Vγ9Vδ2 T cells in the control of mycobacterial infection. Copyright © 2007 by The American Association of Immunologists, Inc.