AIM: To investigate the role of MHC classⅡin the modulation of gastric epithelial cell apoptosis induced by H pylon infection. METHODS: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specific for MHC classⅡand CD95, the quantitation of apoptotic and anti-apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a fluorometric assay, a cytometric bead array, and confocal microscopy, respectively. RESULTS: Pretreatment of N87 cells with the anti-MHC classⅡIgM antibody RFD1 resulted in a reduction in global caspase activation at 24 h of H pylori infection. When caspase 3 activation was specifically measured, crosslinking of MHC class n resulted in markedly reduced caspase activation, while simple ligation of MHC classⅡdid not. Crosslinking of MHC class n also resulted in an increased activation of the anti-apoptosis molecule BCL-2 compared to simple ligation. Confocal microscope analysis demonstrated that the pretreatment of gastric epithelial cells with a crosslinking anti-MHC classⅡIgM blocked the recruitment of FADD to the cell surface. CONCLUSION: The ability of MHC class n to modulate gastric epithelial apoptosis is at least partially dependent on its crosslinking. The crosslinking of this molecule has anti-apoptotic effects during the earlier time points of H pylori infection. This effect is possibly mediated by the ability of MHC classⅡto modulate the activation of the pro-apoptotic receptor Fas by blocking the recruitment of the accessory molecule FADD, and this delay in apoptosis induction could allow for prolonged cytokine secretion by H pylori-infected gastric epithelial cells. AIM: To investigate the role of MHC class II in the modulation of gastric epithelial cell apoptosis induced by H pylon infection. METHODS: After stimulating a human gastric epithelial cell line with bacteria or agonist antibodies specific for MHC class II and CD95, the quantitation of apoptotic and anti- apoptotic events, including caspase activation, BCL-2 activation, and FADD recruitment, was performed with a fluorometric assay, a cytometric bead array, and confocal microscopy, respectively. RESULTS: Pretreatment of N87 cells with the anti-MHC class II IgG antibody RFD1 resulted in a reduction in caspase activation at 24 h of H pylori infection. When caspase 3 activation was specifically measured, crosslinking of MHC class n resulted in markedly reduced caspase activation, while simple ligation of MHC class II did not. Crosslinking of MHC class n also resulted in an increased activation of the anti-apoptosis molecule BCL-2 compared to simple ligation. Confocal microscope analysis d emonstrated that the pretreatment of gastric epithelial cells with a crosslinking anti-MHC class II IgG blocked by the recruitment of FADD to the cell surface. CONCLUSION: The ability of MHC class n to modulate gastric epithelial apoptosis is at least partially dependent on its crosslinking. this molecule has anti-apoptotic effects during the earlier time points of H pylori infection. This effect is possibly mediated by the ability of MHC class II to modulate the activation of the pro-apoptotic receptor Fas by blocking the recruitment of the accessory molecule FADD, and this delay in apoptosis induction could allow for prolonged cytokine secretion by H pylori-infected gastric epithelial cells.