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Vascular cell adhesion molecule-1 induced by human T-cell leukaemia virus type 1 Tax protein in T-cells stimulates proliferation of human T-lymphocytes

Virologie et Pathogénèse Virale (UMR5537), CNRS-UCB Lyon 1, Faculté de Médecine Laennec, Rue Guillaume Paradin, 69372 Lyon Cedex 08, France¹
Immunobiologie Fondamentale et Clinique, INSERM U503, 21 Avenue Tony Garnier, 69365 Lyon Cedex 07, France²

Author for correspondence: Hélène Valentin at INSERM. Fax +33 4 37 28 23 41. e-mail valentin{at}cervi-lyon.inserm.fr

Human T-cell leukaemia/lymphotropic virus type 1 (HTLV-1), aetiologically linked to lymphoproliferative as well as inflammatory diseases, infects and activates CD4⁺ helper T-cells and thus alters immunoregulatory pathways. The viral regulatory Tax protein has been shown previously to induce the expression of vascular cell adhesion molecule-1 (VCAM-1) by T-cells. To determine the functional role of this adhesion molecule, Jurkat T-cells stably expressing either Tax or both Tax and Rex (another viral regulatory protein) were used in binding and coculture assays performed with either control Jurkat cells or primary human T-lymphocytes. Evidence was provided that VCAM-1 acting in synergy with leucocyte function-associated antigen-3 promotes T-cell–T-cell interactions and increases T-cell proliferation. Interestingly, Rex was found to modulate these events. These data establish that VCAM-1 induced by Tax on T-cells thus contributes to the immunopathological process triggered by HTLV-1 infection.