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 Vδ 1 T cells and Vδ 2 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 Vδ 2 γδ T cells, skewed toward an activated and terminally differentiated effector memory phenotype T EMRA Vδ 2 γδ T cell, which may account for the dysfunction of Vδ 2 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 Vδ 2 T cells during HIV pathogenesis and represent a sound basis on which to consider immune therapies with these cells.
Original language | English (US) |
---|---|
Pages (from-to) | 604-614 |
Number of pages | 11 |
Journal | Cellular and Molecular Immunology |
Volume | 12 |
Issue number | 5 |
DOIs | |
State | Published - Sep 8 2015 |
Externally published | Yes |
Keywords
- HIV
- IL-17
- immune activation
- memory V δ<inf>2</inf>γδ T cells
- γδT cell
ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases
- Immunology