Does h pylori receptor MHC class II contribute to the dynamic gastric epithelial apoptotic response?
The ability of MHC class II 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 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.
The nonresponder phenomenon is present from birth on and genetically determined. In our population, it was not associated with age or the presence of atopy, and appeared not to be caused by mutations in the Fc(epsilon)RI beta-chain.