Staphylococcal enterotoxin B-specific adhesion of murine splenic T cells to a human endothelial cell line

The presence of a putative autoantigen of autoimmune disorder in a target organ may cause accumulation of specific T cells in the inflammatory region. One of the mechanisms of such accumulation involves the migration of specific-circulating T cells through the endothelial cells into the target lesion. The presence of only a few specific T cells responsive to a putative autoantigen has hampered the investigation of specific migration of circulating T cells to the target organ. We used a superantigen to investigate specific T-cell adhesion to endothelial cells, because it stimulates a large proportion of T cells with particular V beta elements and adhesion of T cells to the endothelium is a vital step in the migration process. Adhesion of murine T cells to the human endothelial cell line, EA.hy926, was specifically increased in the presence of staphylococcal enterotoxin B (SEE). The increase was interferon-gamma (IFN-gamma)-dependent, and consisted mainly of CD4(+) T cells. V beta 8.1,2(+) T cells preferentially adhered to endothelial cells in the presence of SEE compared with V beta 6(+) T cells. Pretreatment of endothelial cells with SEE increased the adherence of V beta 8.1,2(+) T cells, while anti-human leucocyte antigen (HLA)-DR and -DQ antibodies inhibited the increased adherence of V beta 8.1,2(+) T cells. Our results demonstrate that increased T-cell adhesion to endothelial cells is' SEE specific, and that the specificity is dependent on major histocompatibility complex (MHC) class II molecules expressed on endothelial cells' and on the recognition of the SEB-MHC class II complex by V beta 8.1,2(+) T cells.