Journal
FRONTIERS IN IMMUNOLOGY
Volume 7, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2016.00579
Keywords
HIV-1; double-negative T cell; immune reconstitution; immune activation; antiretroviral therapy; TGF-beta 1
Categories
Funding
- Beijing Municipal of Science and Technology Major Project [D141100000314005, D161100000416003]
- National Natural Science Foundation of China [81501732]
- Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support [ZY201401]
- Beijing Key Laboratory for HIV/AIDS Research [BZ0089]
- Funding for Chinese overseas talents returning to China
- Sidaction
- ANRS (French National Agency for Research on AIDS and Viral hepatitis)
Ask authors/readers for more resources
Failure of immune reconstitution increases the risk of AIDS or non-AIDS related morbidity and mortality in HIV-1-infected patients. CD3(+)CD4(-)CD8(-) T cells, which are usually described as double-negative (DN) T cells, display CD4-like helper and immunoregulatory functions. Here, we have measured the percentage of DN T cells in the immune reconstituted vs. non-immune reconstituted HIV-1-infected individuals. We observed that immunological non-responders (INRs) had a low number of DN T cells after long-term antiretroviral therapy (ART), and the number of these cells positively correlated with the CCM+ T cell count. The ART did not result in complete suppression of immune activation recorded by the percentage of CD38(+)HLA-DR(+)CD8(+) T cells in INRs, and a strong inverse correlation was observed between DN T cells and immune activation. A low proportion of TGF-beta 1(+)UN T cells was found in INRs. Further mechanism study demonstrated that the level of TGF-beta 1-producing DN T cells and immune activation had a negative correlation after ART. Taken together, our study suggests that DN T cells control the immunological response in HIV-1-infected patients. These findings expand our understanding of the mechanism of immune reconstitution and could develop specific treatments to return the immune system to homeostasis following initiation of HIV-1 therapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available