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Blood, 25 June 2009, Vol. 113, No. 26, pp. 6611-6618.
Prepublished online as a Blood First Edition Paper on April 24, 2009; DOI 10.1182/blood-2009-01-198028.
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IMMUNOBIOLOGY
V 1 T lymphocytes producing IFN- and IL-17 are expanded in HIV-1–infected patients and respond to Candida albicans
Daniela Fenoglio1,
Alessandro Poggi2,
Silvia Catellani3,
Florinda Battaglia1,
Alessandra Ferrera1,
Maurizio Setti4,
Giuseppe Murdaca5, and
Maria Raffaella Zocchi6
1 Centre of Excellence for Biological Sciences, University of Genoa, Genoa;
2 Laboratory of Immunology, National Institute for Cancer Research, Genoa;
3 Laboratory of Hematology, Department of Internal Medicine,
4 Department of Internal Medicine, and
5 Department of Semiotics, University of Genoa, Genoa; and
6 Division of Immunology, Transplants, and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy
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 V 1 T cells display cytoplasmic interferon- (IFN- ). Interestingly, these cells coexpress cytoplasmic interleukin-17 (IL-17), and bear the CD27 surface marker of the memory T-cell subset. V 1 T cells, isolated from either patients or healthy donors, can proliferate and produce IFN- and IL-17 in response to Candida albicans in vitro, whereas V 2 T cells respond with proliferation and IFN- /IL-17 production to mycobacterial or phosphate antigens. These IFN- /IL-17 double-producer  T cells express the Th17 RORC and the Th1 TXB21 transcription factors and bear the CCR7 homing receptor and the CD161 molecule that are involved in  T-cell transendothelial migration. Moreover, V 1 T cells responding to C albicans express the chemokine 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 defense against opportunistic infections, possibly contributing to compensate for the impairment of CD4+ T cells.

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