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Engagement of specific T-cell surface molecules regulates cytoskeletal polarization in HTLV-1-infected lymphocytes

Amanda L Barnard1, Tadahiko Igakura, Yuetsu Tanaka

  • 1Department of Immunology, Wright-Fleming Institute, Imperial College London, St Mary's Campus, London W2 1PG, United Kingdom.

Blood
|April 16, 2005
PubMed

Insights

Human T-lymphotropic virus type 1 (HTLV-1) uses intercellular adhesion molecule-1 (ICAM-1) to enhance cell-to-cell transmission. A positive feedback loop between ICAM-1 and HTLV-1 Tax protein drives virologic synapse formation and T-cell tropism.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Efficient transmission of human T-lymphotropic virus type 1 (HTLV-1) relies on cell-cell contact.
  • HTLV-1-infected cells polarize their microtubule-organizing center (MTOC) towards junctions, accumulating viral components for transfer.

Purpose of the Study:

  • To investigate the role of T-cell surface ligands in HTLV-1-induced MTOC polarization.
  • To test if T-cell surface ligand engagement synergizes with HTLV-1 infection to cause MTOC polarization.

Main Methods:

  • Utilized antibodies against intercellular adhesion molecule-1 (ICAM-1; CD54), CD3, and CD28.
  • Assessed MTOC polarization frequency in HTLV-1-infected and uninfected T cells.
  • Measured HTLV-1 gene expression in response to ICAM-1 upregulation.

Main Results:

  • Antibodies to ICAM-1 significantly increased MTOC polarization in HTLV-1-infected cells.
  • HTLV-1 infection upregulates ICAM-1 expression on infected cells.
  • ICAM-1 upregulation on the cell surface enhances HTLV-1 gene expression.
  • HTLV-1 infection inhibited MTOC polarization induced by CD3 or CD28 antibodies.

Conclusions:

  • A positive feedback loop between ICAM-1 and HTLV-1 Tax protein facilitates virologic synapse formation.
  • This ICAM-1/Tax interaction contributes to HTLV-1's specific tropism for T cells.

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