Vδ1 T lymphocytes producing IFN-γ and IL-17 are expanded in HIV-1-infected patients and respond to Candida albicans

被引:142
作者
Fenoglio, Daniela [2 ]
Poggi, Alessandro [1 ]
Catellani, Silvia [3 ]
Battaglia, Florinda [2 ]
Ferrera, Alessandra [2 ]
Setti, Maurizio
Murdaca, Giuseppe [4 ]
Zocchi, Maria Raffaella [5 ]
机构
[1] Natl Inst Canc Res, Immunol Lab, I-16132 Genoa, Italy
[2] Univ Genoa, Ctr Excellence Biol Sci, Genoa, Italy
[3] Univ Genoa, Dept Internal Med, Hematol Lab, I-16126 Genoa, Italy
[4] Univ Genoa, Dept Semiot, I-16126 Genoa, Italy
[5] Ist Sci San Raffaele, Div Immunol Transplants & Infect Dis, I-20132 Milan, Italy
关键词
MYCOBACTERIUM-TUBERCULOSIS INFECTION; MULTIPLE-SCLEROSIS PATIENTS; HEALTHY DONORS; DELTA CELLS; IN-VIVO; ACQUIRED-IMMUNITY; TNF-ALPHA; TIME; RECEPTOR; INNATE;
D O I
10.1182/blood-2009-01-198028
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In early HIV-1 infection, V delta 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 delta 1 T cells display cytoplasmic interferon-gamma (IFN-gamma). Interestingly, these cells coexpress cytoplasmic interleukin-17 (IL-17), and bear the CD27 surface marker of the memory T-cell subset. V delta 1 T cells, isolated from either patients or healthy donors, can proliferate and produce IFN-gamma and IL-17 in response to Candida albicans in vitro, whereas V delta 2 T cells respond with proliferation and IFN-gamma/IL-17 production to mycobacterial or phosphate antigens. These IFN-gamma/IL-17 double-producer gamma delta 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 gamma delta T-cell transendothelial migration. Moreover, V delta 1 T cells responding to C albicans express the chemokine receptors CCR4 and CCR6. This specifically equipped circulating memory gamma delta 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. (Blood. 2009; 113: 6611-6618)
引用
收藏
页码:6611 / 6618
页数:8
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