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Active Epstein (active + epstein)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Active Epstein

  • chronic active epstein
    		•

    Selected Abstracts

    Optimal treatment for chronic active Epstein,Barr virus disease

    PEDIATRIC TRANSPLANTATION, Issue 4 2009
    Jeffrey I. Cohen
    First page of article [source]

    Chronic active Epstein,Barr virus , Is it real and how do you treat it?

    PEDIATRIC TRANSPLANTATION, Issue 2 2009
    Thomas G. Gross
    No abstract is available for this article. [source]

    Marked swollen erythema of the face together with sicca syndrome as a sign for chronic active Epstein,Barr virus infection

    BRITISH JOURNAL OF DERMATOLOGY, Issue 6 2000
    K.C. Sato-Matsumura
    No abstract is available for this article. [source]

    Adhesion of Epstein,Barr virus-positive natural killer cell lines to cultured endothelial cells stimulated with inflammatory cytokines

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2008
    H. Kanno
    Summary Chronic active Epstein,Barr virus (EBV) infection (CAEBV) is characterized by chronic recurrent infectious mononucleosis-like symptoms. Approximately one-fourth of CAEBV patients develop vascular lesions with infiltration of EBV-positive lymphoid cells. Furthermore, EBV-positive natural killer (NK)/T cell lymphomas often exhibit angiocentric or angiodestructive lesions. These suggest an affinity of EBV-positive NK/T cells to vascular components. In this study, we evaluated the expression of adhesion molecules and cytokines in EBV-positive NK lymphoma cell lines, SNK1 and SNK6, and examined the role of cytokines in the interaction between NK cell lines and endothelial cells. SNKs expressed intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) at much higher levels than those in EBV-negative T cell lines. SNKs produced the larger amount of tumour necrosis factor (TNF)-,, which caused increased expression of ICAM-1 and VCAM-1 in cultured human endothelial cells, than that from EBV-negative T cell lines. Furthermore, SNKs exhibited increased adhesion to cultured endothelial cells stimulated with TNF-, or interleukin (IL)-1,, and the pretreatment of cytokine-stimulated endothelial cells with anti-VCAM-1-antibodies reduced cell adhesion. These indicate that the up-regulated expression of VCAM-1 on cytokine-stimulated endothelial cells would be important for the adhesion of EBV-positive NK cells and might initiate the vascular lesions. [source]