title: HLA-DR expression on regulatory T cells is closely associated with the global immune activation in HIV-1 infected subjects naïve to antiretroviral therapy.
abstract: BACKGROUND
  The frequencies of regulatory T cells (Tregs) increased over the HIV infection but its counts actually decreased. We proposed that the decrease of Treg counts may cause the reduction of inhibitory effect and thereby account for the over-activation of Tregs during HIV infection. However, it remains unknown whether Tregs are also over-activated and thereafter the activation induced death may lead to the decrease of Tregs.
  
  
  METHODS
  Tregs were defined as CD4(+)CD25(+)CD127(lo/-) T cells. Eighty-one HIV-1 infected patients were enrolled in our study, and twenty-two HIV-1 seronegative donors were recruited as the control. The levels of HLA-DR on Tregs were determined by FACSAria flow cytometer.
  
  
  RESULTS
  Compared to HIV-1 seronegative donors, the levels of HLA-DR on CD4(+)CD25(+)CD127(lo/-) Tregs were significantly increased in HIV-1 infected patients, and its increase was positively associated with viral loads (r = 0.3163, P = 0.004) and negatively with CD4 T-cell counts (r = -0.4153, P < 0.0001). In addition, significant associations between HLA-DR expression on CD4(+)CD25(+)CD127(lo/-) Tregs and the percentages of HLA-DR, CD38, Ki67 expressing CD4(+) and CD8(+) T cells were also identified.
  
  
  CONCLUSIONS
  HLA-DR on Tregs is a good marker for viral replication and disease progression. The over-activation of Tregs might result in the decrease of Tregs.
authors.affiliation: Department of Microbiology, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, Sichuan 610041, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Xiao
authors.forename: Ke-lei
authors.initials: KL
authors.lastname: Qian
authors.forename: Qing-hua
authors.initials: QH
authors.lastname: Cao
authors.forename: Chen-li
authors.initials: CL
authors.lastname: Qiu
authors.forename: Cao
authors.initials: C
authors.lastname: Qiu
authors.forename: Yi-le
authors.initials: YL
authors.lastname: Xue
authors.forename: Xiao-yan
authors.initials: XY
authors.lastname: Zhang
authors.forename: Ping
authors.initials: P
authors.lastname: Zhong
authors.forename: Jian-qing
authors.initials: JQ
authors.lastname: Xu
authors.forename: Ming-yuan
authors.initials: MY
authors.lastname: Li
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000378:metabolism; D000328:Adult; D000368:Aged; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D002478:Cells, Cultured; D005260:Female; D005434:Flow Cytometry; D015658:HIV Infections / Q000276:immunology* / Q000378:metabolism*; D006684:HLA-DR Antigens / Q000378:metabolism*; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D053699:Interleukin-7 Receptor alpha Subunit / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism*; D055815:Young Adult
chemical_list: D006684:HLA-DR Antigens; D053645:Interleukin-2 Receptor alpha Subunit; D053699:Interleukin-7 Receptor alpha Subunit; D051997:ADP-ribosyl Cyclase 1