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Blood, 1 August 2005, Vol. 106, No. 3, pp. 988-995.
Prepublished online as a Blood First Edition Paper on April 14, 2005; DOI 10.1182/blood-2004-07-2850.
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IMMUNOBIOLOGY
Engagement of specific T-cell surface molecules regulates cytoskeletal polarization in HTLV-1–infected lymphocytes
Amanda L. Barnard,
Tadahiko Igakura,
Yuetsu Tanaka,
Graham P. Taylor, and
Charles R.M. Bangham
From the Department of Immunology, Wright-Fleming Institute, Imperial College London, St Mary's Campus, London, United Kingdom; the Department of Genito-Urinary Medicine and Communicable Diseases, Wright-Fleming Institute, Imperial College London, St Mary's Campus, London, United Kingdom; and the Department of Infectious Disease and Immunology, Okinawa-Asia Research Center of Medical Science, Faculty of Medicine, University of the Ryukus, Nishihara, Okinawa, Japan.
Cell-cell contact is required for efficient transmission of human T-lymphotropic virus type 1 (HTLV-1). An HTLV-1–infected cell polarizes its microtubule-organizing center (MTOC) toward the cell-cell junction; HTLV-1 core (Gag) complexes and the HTLV-1 genome accumulate at the point of contact and are then transferred to the uninfected cell. However, the mechanisms involved in this cytoskeletal polarization and transport of HTLV-1 complexes are unknown. Here, we tested the hypothesis that engagement of a specific T-cell surface ligand is synergistic with HTLV-1 infection in causing polarization of the MTOC to the cell contact region. We show that antibodies to intercellular adhesion molecule-1 (ICAM-1; CD54) caused MTOC polarization at a higher frequency in HTLV-1–infected cells. ICAM-1 is upregulated on HTLV-1–infected cells, and, in turn, ICAM-1 on the cell surface upregulates HTLV-1 gene expression. We propose that a positive feedback loop involving ICAM-1 and HTLV-1 Tax protein facilitates the formation of the virologic synapse and contributes to the T-cell tropism of HTLV-1. In contrast, MTOC polarization induced in T cells by antibodies to CD3 or CD28 was significantly inhibited by HTLV-1 infection.
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