title: The decrease of regulatory T cells correlates with excessive activation and apoptosis of CD8+ T cells in HIV-1-infected typical progressors, but not in long-term non-progressors.
abstract: Persistent HIV infection results in a decrease in absolute counts of CD4(+) CD25(+) regulatory T cells (Treg). To investigate the role of decreased Treg counts in the regulation of excessive activation and apoptosis of CD8(+) T cells in human immunodeficiency virus (HIV)-1 infection, we characterized Treg in 83 HIV-1-infected individuals, including 19 long-term non-progressors (LTNPs) and 51 typical progressors (TPs) who were treatment-naïve, and 13 AIDS patients on highly active antiretroviral therapy (HAART), of whom nine were complete responders (CRs) and the remaining four were non-responders (NRs) to the treatment. TPs but not LTNPs had a significant decrease in absolute counts of circulating Treg, which was inversely correlated with the activation and apoptosis of CD8(+) T cells. Efficient HAART was found to increase Treg counts in CR patients and temper the excessive activation and apoptosis of CD8(+) T cells. Moreover, isolated Treg significantly inhibited the spontaneous and anti-CD3-induced apoptosis of CD8(+) T cells in a dose-dependent manner in vitro. Thus, our findings indicate that the decrease in Treg closely correlates with the increase in apoptotic CD8(+) T cells and disease progression in chronic HIV-1 infection, and that Treg may play a key role in maintaining the balance between the amount and quality of CD8(+) T cells in HIV-1 infection. Manipulation of Treg function may be a promising strategy for immune therapy of this disease.
authors.affiliation: Department of Infectious Diseases, Beijing You-an Hospital Affiliated to Capital Medical University, Beijing, China.
authors.forename: Yanmei
authors.initials: Y
authors.lastname: Jiao
authors.forename: JunLiang
authors.initials: J
authors.lastname: Fu
authors.forename: Shaojun
authors.initials: S
authors.lastname: Xing
authors.forename: Baoyun
authors.initials: B
authors.lastname: Fu
authors.forename: Zheng
authors.initials: Z
authors.lastname: Zhang
authors.forename: Ming
authors.initials: M
authors.lastname: Shi
authors.forename: Xicheng
authors.initials: X
authors.lastname: Wang
authors.forename: Jiyuan
authors.initials: J
authors.lastname: Zhang
authors.forename: Lei
authors.initials: L
authors.lastname: Jin
authors.forename: Fubiao
authors.initials: F
authors.lastname: Kang
authors.forename: Hao
authors.initials: H
authors.lastname: Wu
authors.forename: Fu-Sheng
authors.initials: FS
authors.lastname: Wang
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use; D023241:Antiretroviral Therapy, Highly Active; D017209:Apoptosis / Q000276:immunology; D018791:CD4 Lymphocyte Count; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000821:virology; D002908:Chronic Disease; D018450:Disease Progression; D005260:Female; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology* / Q000821:virology; D015497:HIV-1; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000821:virology
chemical_list: D019380:Anti-HIV Agents; D012367:RNA, Viral