TY - JOUR
T1 - Phosphoantigen-expanded human γδ T cells display potent cytotoxicity against monocyte-derived macrophages infected with human and avian influenza viruses
AU - Qin, Gang
AU - Mao, Huawei
AU - Zheng, Jian
AU - Sia, Sin Fun
AU - Liu, Yinping
AU - Chan, Ping Lung
AU - Lam, Kwok Tai
AU - Malik Peiris, J. S.
AU - Lau, Yu Lung
AU - Tu, Wenwei
N1 - Funding Information:
Financial support: Research Grants Council of Hong Kong (General Research Fund; grants HKU 777407M and HKU 777108M to W.T.); Research Fund for the Control of Infectious Diseases, Hong Kong government (grant 07060482 to W.T.); University Grants Committee, Hong Kong (grant AoE/M-12/06 to Y.-L.L. and W.T.); University of Hong Kong (postgraduate studentships to G.Q., H.M., J.Z., and P.-L.C.); Edward Sai Kim Hotung Paediatric Education and Research Fund (G.Q., H.M., J.Z., and P.-L.C.).
PY - 2009/9/15
Y1 - 2009/9/15
N2 - Background. Influenza virus is a cause of substantial annual morbidity and mortality worldwide. The potential emergence of a new pandemic strain (eg, avian influenza virus) is a major concern. Currently available vaccines and anti-influenza drugs have limited effectiveness for influenza virus infections, especially for new pandemic strains. Therefore, there is an acute need to develop alternative strategies for influenza therapy, γδ T cells have potent antiviral activities against different viruses, but no data are available concerning their antiviral activity against influenza viruses. Methods. In this study, we used virus-infected primary human monocyte-derived macrophages (MDMs) to examine the antiviral activity of phosphoantigen isopentenyl pyrophosphate (IPP)-expanded human Vγ9Vδ2 T cells against influenza viruses. Results. Vγ9Vδ2 T cells were selectively activated and expanded by IPP from peripheral blood mononuclear cells. IPP-expanded Vγ9Vδ2 T cells efficiently killed MDMs infected with human (H1N1) or avian (H9N2 or H5N1) influenza virus and significantly inhibited viral replication. The cytotoxicity of Vγ9Vδ2 T cells against influenza virus-infected MDMs was dependent on NKG2D activation and was mediated by Fas-Fas ligand and perforin-granzyme B pathways. Conclusion. Our findings suggest a potentially novel therapeutic approach to seasonal, zoonotic avian, and pandemic influenza-the use of phosphoantigens to activate γδ T cells against influenza virus infections.
AB - Background. Influenza virus is a cause of substantial annual morbidity and mortality worldwide. The potential emergence of a new pandemic strain (eg, avian influenza virus) is a major concern. Currently available vaccines and anti-influenza drugs have limited effectiveness for influenza virus infections, especially for new pandemic strains. Therefore, there is an acute need to develop alternative strategies for influenza therapy, γδ T cells have potent antiviral activities against different viruses, but no data are available concerning their antiviral activity against influenza viruses. Methods. In this study, we used virus-infected primary human monocyte-derived macrophages (MDMs) to examine the antiviral activity of phosphoantigen isopentenyl pyrophosphate (IPP)-expanded human Vγ9Vδ2 T cells against influenza viruses. Results. Vγ9Vδ2 T cells were selectively activated and expanded by IPP from peripheral blood mononuclear cells. IPP-expanded Vγ9Vδ2 T cells efficiently killed MDMs infected with human (H1N1) or avian (H9N2 or H5N1) influenza virus and significantly inhibited viral replication. The cytotoxicity of Vγ9Vδ2 T cells against influenza virus-infected MDMs was dependent on NKG2D activation and was mediated by Fas-Fas ligand and perforin-granzyme B pathways. Conclusion. Our findings suggest a potentially novel therapeutic approach to seasonal, zoonotic avian, and pandemic influenza-the use of phosphoantigens to activate γδ T cells against influenza virus infections.
UR - http://www.scopus.com/inward/record.url?scp=70349417911&partnerID=8YFLogxK
U2 - 10.1086/605413
DO - 10.1086/605413
M3 - Article
C2 - 19656068
AN - SCOPUS:70349417911
SN - 0022-1899
VL - 200
SP - 858
EP - 865
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 6
ER -