Expression and activation of a C-terminal truncated isoform of STAT5 (STAT5Δ) following interleukin 2 administration or AZT monotherapy in HIV-infected individuals

Chiara Bovolenta, Laura Camorali, Massimiliano Mauri, Silvia Ghezzi, Silvia Nozza, Giuseppe Tambussi, Adriano Lazzarin, Guido Poli

Research output: Contribution to journalArticlepeer-review

Abstract

Intermittent administration of recombinant interleukin-2 (rIL-2) to individuals infected with human immunodeficiency virus (HIV) has been shown to raise and maintain the absolute number of circulating CD4+ T cells to normal or near normal levels. One of the signaling pathways triggered by IL-2 is the Janus kinase-signal transducer and activator of transcription (JAK-STAT). In particular, IL-2 activates the tyrosine kinases JAK1 and JAK3 and the transcription factors STAT3 and STAT5. We have previously observed that most HIV+ individuals, unlike healthy seronegative controls, show a constitutive activation of STAT1 and a C-terminal truncated isoform of STAT5 (STAT5Δ). In the present study, we have analyzed the protein level and activation state of STAT5 isoforms expressed in peripheral blood mononuclear cells of two HIV-infected individuals who showed a good or a poor response to intermittent IL-2 administration, respectively, and of a single individual before and after initiation of Zidovudine monotherapy. We provide evidence that both therapeutic interventions enhanced the expression and activation of the C-terminal truncated isoform of STAT5 (STAT5Δ) in vivo.

Original languageEnglish
Pages (from-to)75-81
Number of pages7
JournalClinical Immunology
Volume99
Issue number1
DOIs
Publication statusPublished - 2001

Keywords

  • AIDS/HIV
  • AZT
  • IL-2
  • Immunotherapy
  • STAT

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Pathology and Forensic Medicine

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