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 naıve 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/μL 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 naıve 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.

Conclusion. Our results suggest to not use steroid therapy as adjuvant immunotherapy in patients with less than optimal immunologic response to HAART.