3 results match your criteria: "Franche-Comte School of Medicine[Affiliation]"
J Leukoc Biol
March 2008
Franche-Comté School of Medicine, Hôpital Saint-Jacques, 2 Place Saint-Jacques, F-25030 Besançon Cedex, France.
HIV-1 two-exon transactivator protein (Tat) is a 101-aa protein. We investigated the possible contribution of the extreme C terminus of HIV-1 Tat to maximize nuclear transcription factor NF-kappaB activation, long terminal repeat (LTR) transactivation, and viral replication in T cells. C-terminal deletion and substitution mutants made with the infectious clone HIV-89.
View Article and Find Full Text PDFImmunology
July 2007
Department of Virology, Franche-Comte School of Medicine, Besançon, France.
CD8(+) T cells provide protective immune responses via both cytolytic and non-cytolytic mechanisms in subjects infected with human immunodeficiency virus (HIV). In the present study, we investigated the CD28 expression of CD8(+) T cells present in the peripheral blood lymphocyte subset isolated from chronically HIV-infected subjects. Using flow cytometric analysis, a continuous spectrum of CD28 intensity ranging from negative to high, which could be separated into CD28-negative, intermediate (int) and high, was seen for CD8(+) T cells.
View Article and Find Full Text PDFJ Gen Virol
June 2004
Department of Virology and Institut d'Etude et de Transfert de Genes, University of Franche-Comte School of Medicine, Hôpital Saint-Jacques, 2 place Saint-Jacques, F-25030 Besançon cedex, France.
Mechanisms of CXCR4-mediated T lymphocyte apoptosis in human immunodeficiency virus (HIV) infection are poorly understood. The authors used peripheral blood mononuclear cells isolated from HIV type 1-infected subjects and assessed both CD4(+) and CD8(+) T cell apoptosis in the presence and absence of CXCR4 blockade by AMD3100. Both CD4(+) and CD8(+) T cell apoptosis could be inhibited by CXCR4 blockade, mostly in acquired immunodeficiency syndrome subjects and more weakly in asymptomatic HIV-positive subjects, and depended only partially on the syncytium-inducing/non-syncytium-inducing viral envelope phenotype.
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