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CD30 induction of human immunodeficiency virus gene transcription is mediated by TRAF2

E N Tsitsikov1, D A Wright, R S Geha

  • 1Division of Immunology, Children's Hospital, Department of Pediatrics Harvard Medical School, Boston, MA 02115, USA.

Proceedings of the National Academy of Sciences of the United States of America
|February 18, 1997
PubMed

Insights

CD30 receptor ligation activates NF-kappaB and enhances HIV expression through TRAF-2 signaling in T lymphocytes. This study identifies TRAF2 as a key mediator in CD30-induced HIV transcription.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • CD30, a TNFR superfamily member, is expressed on immune cells.
  • CD30 ligation is known to activate NF-kappaB and increase HIV expression.

Purpose of the Study:

  • To investigate the role of TRAF proteins in CD30-mediated signaling.
  • To elucidate the mechanism by which CD30 ligation affects HIV expression.

Main Methods:

  • Studied TRAF1 and TRAF2 binding to the intracellular domain of CD30 (CD30IC).
  • Utilized transient overexpression and dominant-negative mutants in KT3 T cell lines.
  • Assessed NF-kappaB activation and HIV-1 long terminal repeat-driven transcription.

Main Results:

  • TRAF1 and TRAF2 bind to CD30IC.
  • TRAF2 overexpression, but not TRAF1, induced NF-kappaB activation and HIV-1 transcription.
  • Dominant-negative TRAF mutants inhibited CD30-induced NF-kappaB activation and HIV-1 transcription.

Conclusions:

  • CD30 signaling enhances HIV expression via TRAF-2-mediated NF-kappaB activation.
  • TRAF2 is a critical component in the CD30-induced pathway for HIV transcription.

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