Submitted January 7, 2009
Accepted April 19, 2009
V
1 T lymphocytes producing IFN
and IL-17 are expanded in HIV-1 infected patients and respond to Candida albicans
Daniela Fenoglio, Alessandro Poggi*, Silvia Catellani, Florinda Battaglia, Alessandra Ferrera, Maurizio Setti, Giuseppe Murdaca, and Maria Raffaella Zocchi
CEBR, University of Genoa, Genoa, Italy
Laboratory of Immunology, National Institute for Cancer Research, Genoa, Italy
Laboratory of Hematology , DIMI, University of Genoa, Genoa, Italy
Department of Internal Medicine, University of Genoa, Genoa, Italy
Department of Semiotics, University of Genoa, Genoa, Italy
Laboratory of Tumor Immunology, San Raffaele Scientific Institute, Milan, Italy
* Corresponding author; email: alessandro.poggi{at}istge.it.
In early HIV-1 infection V
1 T lymphocytes are increased in peripheral blood and this is related to chemokine receptor expression, chemokine response and recirculation. Herein we show that, at variance with healthy donors, in HIV-1 infected patients ex-vivo isolated V1 T cells display cytoplasmic interferon (IFN)-
. Interestingly, these cells co-express cytoplasmic interleukin (IL)-17, and bear the CD27 surface marker of the memory T cell subset. V1 T cells, isolated from either patients or healthy donors, can proliferate and produce IFN- and IL-17 in response to Candida albicans in vitro, while V2 T cells respond with proliferation and IFN-/IL-17 production to mycobacterial or phosphate antigens. These IFN-/IL-17 double producers T cells express the Th17 RORC and the Th1 TXB21 transcription factors, bear the CCR7 homing receptor and the CD161 molecule, involved in T cell transendothelial migration. Moreover, V1 T cells responding to C. albicans express the chemochine receptors CCR4 and CCR6.
This specifically equipped circulating memory T cell population might play an important role in the control of HIV-1 spreading and in the defence against opportunistic infections, possibly contributing to compensate the impairment of CD4+ T cells.
