Central memory Vgamma9Vdelta2 T lymphocytes primed and expanded by bacillus Calmette-Guérin-infected dendritic cells kill mycobacterial-infected monocytes
Martino, A.; Casetti, R.; Sacchi, A.; Poccia, F.
Journal of Immunology 179(5): 3057-3064
2007
ISSN/ISBN: 0022-1767 PMID: 17709520 Document Number: 613145
In humans, innate immune recognition of mycobacteria, including Mycobacterium tuberculosis and bacillus Calmette-Guerin (BCG), is a feature of cells as dendritic cells (DC) and gamma delta T cells. In this study, we show that BCG infection of human monocyte-derived DC induces a rapid activation of V gamma 9V delta 2 T cells (the major subset of gamma delta T cell pool in human peripheral blood). Indeed, in the presence of BCG-infected DC, V gamma 9V delta 2 T cells increase both their expression of CD69 and CD25 and the production of TNF-alpha and IFN-gamma, in contrast to DC treated with V gamma 9V delta 2 T cell-specific Ags. Without further exogenous stimuli, BCG-infected DC expand a functionally cytotoxic central memory V gamma 9V delta 2 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 V gamma 9V delta 2 T cells in the control of mycobacterial infection.