title: Apoptosis of naive CD4+ T-cells from HIV-infected patients with poor immune response to HAART is enhanced in vitro by steroid.
abstract: OBJECTIVE
  Because the absence of immune restoration in HIV-infected patients efficiently treated by highly active antiretroviral therapy (HAART) may be due to excessive immune activation, we prospectively studied the effect of hydrocortisone on T-cell apoptosis in a cohort of patients with satisfactory virologic response.
  
  
  METHODS
  Apoptosis of T-cell subsets including naïve CD45RA(+)CD4+ T-cells was determined at baseline and at months 1 and 3 after initiation of HAART. A satisfactory immune response was defined as an increase >100/microL CD4+ T-cells at month 3 compared to baseline.
  
  
  RESULTS
  Twenty out of 63 patients showed undetectable viral load at month 3, among whom eight exhibited a satisfactory immune response. Down-regulation spontaneous CD4+T-cell apoptosis was significant in the group of patients with a satisfactory immune response compared to the other patients. However, hydrocortisone up-regulated apoptosis of naïve CD4+ CD45RA+ T-cells, specifically in group of patients with poor immune response, whatever the time point considered: percentage of apoptotic CD4 T-cells was 16+/-16% without hydrocortisone and 22+/-22% with hydrocortisone at month 1, and respectively, 10+/-9 and 17+/-15% at month 3 (P < 0.05) Hydrocortisone had no impact on CD8+ T-cell apoptosis, whatever the considered group.
  
  
  CONCLUSIONS
  Our results suggest to not use steroid therapy as adjuvant immunotherapy in patients with less than optimal immunologic response to HAART.
authors.affiliation: Service des Maladies Infectieuses et Tropicales, Centre Hospitalier-Universitaire de Nice, Hôpital de l'Archet 1, BP3079, 06202, Nice 3, France. roger.pm@chu-nice.fr
authors.forename: Pierre-Marie
authors.initials: PM
authors.lastname: Roger
authors.forename: Isabelle
authors.initials: I
authors.lastname: Perbost
authors.forename: Michel
authors.initials: M
authors.lastname: Ticchioni
authors.forename: Jean-Gabriel
authors.initials: JG
authors.lastname: Fuzibet
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Breittmayer
authors.forename: Jacques
authors.initials: J
authors.lastname: Durant
authors.forename: Alain
authors.initials: A
authors.lastname: Pesce
authors.forename: Alain
authors.initials: A
authors.lastname: Bernard
authors.forename: Pierre
authors.initials: P
authors.lastname: Dellamonica
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active; D017209:Apoptosis / Q000187:drug effects*; D015704:CD4 Antigens / Q000187:drug effects* / Q000276:immunology; D017024:Chemotherapy, Adjuvant; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D006854:Hydrocortisone / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D016176:T-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology; D019562:Viral Load
chemical_list: D000893:Anti-Inflammatory Agents; D015704:CD4 Antigens; D006854:Hydrocortisone