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

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)‐α, 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‐α or interleukin (IL)‐1β, 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.