Researchers from Italy and the Netherlands investigated the presence of H+, K+-ATPase-specific T-cells in the gastric mucosa of patients with autoimmune gastritis (AIG).
In vivo-activated T-cells from the infiltrates of the gastric mucosa of 5 patients with AIG were isolated and cloned.
The ability of gastric T-cell clones to proliferate and to produce cytokines in response to H+, K+-ATPase was assessed. The team also monitored the cells' expression of B-cell help, perforin-mediated cytotoxicity, and Fas-Fas ligand-mediated apoptosis in target cells.
The researchers found that 25% of the CD4+ clones from the gastric corpus of AIG patients proliferated in response to porcine H+, K+-ATPase.
|25% of T-cell clones proliferated in response to H+, K+-ATPase.|
88% of these clones showed a Th1 profile, whereas a few secreted both Th1 and Th2 cytokines.
Virtually all of the H+, K+-ATPase-specific clones produced tumor necrosis factor alpha and provided substantial help for B-cell immunoglobulin production. In addition, most of the specific clones expressed perforin-mediated cytotoxicity against antigen-presenting cells and induced Fas-Fas ligand-mediated apoptosis in target cells.
Mario M. D'Elios, of the University of Florence, Italy, concluded on behalf of the group, "Activation of proton pump-specific Th1 cytotoxic T-cells in the gastric mucosa can represent an effector mechanism for the target cell destruction in AIG."