## Abstract Recent studies indicate that a defective proliferative response of HIV‐specific CD8+ T cells is associated with the lack of virologic control in chronic HIV infection in humans. The possible mechanisms that might be responsible for the reduced proliferative potential of HIV‐specific CD8
Different rates of CD4+ and CD8+ T-cell proliferation in interleukin-2–treated human immunodeficiency virus-positive subjects
✍ Scribed by Laura Caggiari; Stefania Zanussi; Cinzia Crepaldi; Maria Teresa Bortolin; Cristina Caffau; Monica D'Andrea; Paolo De Paoli
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 137 KB
- Volume
- 46
- Category
- Article
- ISSN
- 0196-4763
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✦ Synopsis
Abstract
BACKGROUND
Interleukin‐2 (IL‐2) has been used successfully to increase CD4 cell counts in patients who are human immunodeficiency virus (HIV) positive. The mechanisms involved in this phenomenon are unknown. We hypothesized that a differential proliferation rate of CD4+ compared with CD8+ lymphocytes could be related to the increase of CD4 counts and of CD4/CD8 ratios that occur in HIV+ patients during IL‐2 treatment.
METHODS
We enrolled in our study 14 HIV+ patients treated with IL‐2 or with highly active antiretroviral therapy (HAART) during a 96‐week observation period. Using flow cytometry, we measured longitudinally the expression of the Ki67 antigen in peripheral blood CD4+ and CD8+ lymphocyte subsets.
RESULTS
Compared with HAART alone, IL‐2 produced a rapid increase of Ki67+ proliferating CD4 cells and a concomitant increase of the CD4/CD8 ratios, whereas the corresponding CD8 proliferation increased slightly. On the contrary, HAART alone was effective in suppressing equally both CD4 and CD8 proliferation.
CONCLUSIONS
Our results suggest a selective activity of IL‐2 on CD4 T‐cell proliferation; on the contrary, CD8‐specific proliferation is affected minimally during treatment. This information may offer the potential to plan correctly immune activating regimens. Cytometry (Comm. Clin. Cytometry) 46:233–237, 2001. © 2001 Wiley‐Liss, Inc.
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