title: T cell activation predicts carotid artery stiffness among HIV-infected women.
abstract: OBJECTIVE
  HIV disease is associated with increased arterial stiffness, which may be related to inflammation provoked by HIV-related immune perturbation. We assessed the association of T cell markers of immune activation and immunosenescence with carotid artery stiffness among HIV-infected women.
  
  
  METHODS
  Among 114 HIV-infected and 43 HIV-uninfected women, we measured CD4+ and CD8+ T cell populations expressing activation (CD38+HLA-DR+) and senescence (CD28-CD57+) markers. We then related these measures of immune status with parameters of carotid artery stiffness, including decreased distensibility, and increased Young's elastic modulus, as assessed by B-mode ultrasound.
  
  
  RESULTS
  HIV infection was associated with increased CD4+ T cell activation, CD8+ T cell activation and CD8+ T cell senescence. Among HIV-infected women, adjusted for age, HIV medications, and vascular risk factors, higher CD4+CD38+HLA-DR+ T cell frequency was associated with decreased carotid artery distensibility (β=-2.00, 95% confidence interval [CI]=-3.86, -0.14, P=0.04) and increased Young's modulus (β=1.00, 95% CI=0.03, 1.97, P=0.04). These associations were affected little by further adjustment for CD4+ T cell count and viral load. Among HIV-infected women, higher frequencies of immunosenescent T cells, including CD4+CD28-CD57+ and CD8+CD28-CD57+ T cells, were also associated with decreased arterial distensibility. Among HIV-uninfected women, frequencies of activated or senescent T cells were not significantly associated with measures of carotid stiffness.
  
  
  CONCLUSIONS
  T cell activation and senescence are associated with arterial stiffness, suggesting that pro-inflammatory populations of T cells may produce functional or structural vascular changes in HIV-infected women.
authors.affiliation: Department of Epidemiology and Population Health, Albert Einstein College of Medicine, USA. rkaplan@aecom.yu.edu
authors.forename: Robert C
authors.initials: RC
authors.lastname: Kaplan
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Sinclair
authors.forename: Alan L
authors.initials: AL
authors.lastname: Landay
authors.forename: Nell
authors.initials: N
authors.lastname: Lurain
authors.forename: A Richey
authors.initials: AR
authors.lastname: Sharrett
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Gange
authors.forename: Xiaonan
authors.initials: X
authors.lastname: Xue
authors.forename: Christina M
authors.initials: CM
authors.lastname: Parrinello
authors.forename: Peter
authors.initials: P
authors.lastname: Hunt
authors.forename: Steven G
authors.initials: SG
authors.lastname: Deeks
authors.forename: Howard N
authors.initials: HN
authors.lastname: Hodis
mesh_terms: D051997:ADP-ribosyl Cyclase 1 / Q000096:biosynthesis; D000328:Adult; D018106:CD28 Antigens / Q000096:biosynthesis; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018959:CD57 Antigens / Q000096:biosynthesis; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D002339:Carotid Arteries / Q000473:pathology*; D016922:Cellular Senescence; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000473:pathology; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D007249:Inflammation; D008213:Lymphocyte Activation; D008875:Middle Aged; D015233:Models, Statistical; D011446:Prospective Studies; D012307:Risk Factors; D013601:T-Lymphocytes / Q000166:cytology*; D059289:Vascular Stiffness
chemical_list: D018106:CD28 Antigens; D018959:CD57 Antigens; D006684:HLA-DR Antigens; D051997:ADP-ribosyl Cyclase 1