来自医学科学院关于γδ T cells的研究

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Cell Mol Immunol. 2014 Sep 15. doi: 10.1038/cmi.2014.77. [Epub ahead of print]

Distortion of memory Vδ2 γδ T cells contributes to immune dysfunction in chronic HIV infection.

Li Z1, Jiao Y2, Hu Y1, Cui L1, Chen D3, Wu H2, Zhang J1, He W1.

Author information

1Department of Immunology, School of Basic Medicine, Peking Union Medical College & Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, State Key Laboratory of Medical Molecular Biology, Beijing, China.
2Beijing Key Laboratory of AIDS, Center for Infectious Diseases, Beijing You'An Hospital, Capital Medical University, Beijing, China.
3Beijing Institute of Liver Disease, Beijing You'An Hospital, Capital Medical University, Beijing, China.


Abstract
γδ T cells play important roles in innate immunity as the first-line of defense against infectious diseases. Human immunodeficiency virus (HIV) infection disrupts the balance between Vδ1 T cells and Vδ2 T cells and causes dysfunction among γδ T cells. However, the biological mechanisms and clinical consequences of this disruption require further investigation. In this study, we performed a comprehensive analysis of phenotype and function of memory γδ T cells in cohorts of Chinese individuals with HIV infection. We found a dynamic change in memory Vδ2 γδ T cells, skewed toward an activated and terminally differentiated effector memory phenotype TEMRA Vδ2 γδ T cell, which may account for the dysfunction of Vδ2 γδ T cells in HIV disease. In addition, we found that IL-17-producing γδ T cells were significantly increased in HIV-infected patients with fast disease progression and positively correlated with HLA-DR+ γδ T cells and CD38+HLA-DR+ γδ T cells. This suggests the IL-17 signaling pathway is involved in γδ T-cell activation and HIV pathogenesis. Our findings provide novel insights into the role of Vδ2 T cells during HIV pathogenesis and represent a sound basis on which to consider immune therapies with these cells.

没有全文，谁可以贡献下。http://www.ncbi.nlm.nih.gov/pubmed/25220734