@entity379 enhances lymphokine-activated killer cell adhesion but not lysis of XXXX .

@entity1 @entity6461 @entity137 @entity5 @entity73179 @entity379 @entity1453 @entity941 @entity1199 @entity2071 @entity213
OBJECTIVES: To determine if treatment with recombinant @entity1 @entity379 ) increases the adhesion to, and lysis of, @entity213 ( @entity6461 ) cells by lymphokine-activated killer (LAK) and peripheral blood mononuclear (PBM) effector cells in vitro and to evaluate the role of cell surface adhesion molecules in these processes. DESIGN: Two @entity1 @entity6461 cell lines, JHU-020- @entity6461 and JHU-022- @entity6461 , were used. Lymphokine-activated killer cells were generated by @entity1199 stimulation of PBM cells obtained from the hemapheresis blood donor packs of healthy individuals. Adhesion assays were performed to assess the level of binding of both effector populations to @entity6461 cells, which were treated with either fresh media or rHuIFN-gamma (100 U/mL). Binding was measured by flow cytometric detection of effector cells labeled with @entity941 -conjugated anti-CD45 monoclonal antibody. Monoclonal antibodies to the cell adhesion molecules HLA-DR, @entity73179 were used in blocking experiments to determine their contribution to the process of effector- @entity6461 cell adhesion. @entity137 experiments were performed using a colorimetric assay to determine the cytotoxic response generated by LAK and PBM cells against @entity6461 cells, with and without prior rHuIFN-gamma treatment of the @entity5 cells. MAIN OUTCOME MEASURES: Effector cell binding level and percent @entity137 of @entity6461 cells. RESULTS: Recombinant @entity1 @entity379 treatment of JHU-020- @entity6461 cells resulted in increased adhesion to both LAK cells and PBM cells (P < .001). The presence of anti- @entity1453 antibody resulted in elimination of the enhanced adhesion seen with rHuIFN-gamma pretreatment of @entity6461 cells (P =.03), but antibody to @entity2071 and HLA-DR did not reduce the level of effector binding. The greatest cytotoxic response against both @entity6461 and JHU-022- @entity6461 was seen with LAK cells (P < or = .001). Pretreatment of @entity5 targets by rHuIFN-gamma (100 U/mL) resulted in no enhancement of cytotoxic response by either LAK or PBM cells; at the effector-target ratio of 30:1, there was a significant decrease in LAK cell-mediated cytotoxic response against rHuIFN-gamma-treated @entity6461 cells (P < or = .02). CONCLUSIONS: Recombinant @entity1 @entity379 treatment of head and neck @entity6461 cells does increase binding of both LAK cells and PBM cells to @entity5 cells, in part via the @entity1453 ligand mechanism. The cytotoxic effect mediated by LAK cells against head and neck @entity6461 cells is reduced after rHuIFN-gamma treatment, suggesting that the activity of this cytokine may be more important in regulating antigen-specific cytotoxic response mediated by cytotoxic T-lymphocytes.
