Immune Reactions Against Elongation Factor 2 Kinase: Specific Pathogenesis of Gastric Ulcer from Helicobacter pylori Infection
Figure 3
Specific cytotoxicity induced by lymphocytes from GU patients. 4 target cells were prepared. (a) HGC-27 cells treated with heat stress and patients’ sera, (b) HGC-27 cells treated with heat stress, (c) HGC-27 cells treated with patients’ sera, (d) nontreated HGC-27 cells. PBMCs were taken from GU patients (). PBMCs stimulated with conA and H. pylori () in addition to IL-12 () or IL-4 () were used as effector cells. Nonstimulated PBMCs () were also used as a control. Both cells reacted with various E/T ratios. An E/T ratio dependent cytotoxicity was observed only against heat-stressed HGC-27 cells or heat-stressed and sera-treated HGC-27 cells. The cytotoxicities of effector cells stimulated by H. pylori lysate were significantly enhanced, regardless of additional cytokine stimulations (*; ). (e) The comparison of cytotoxicities among lymphocytes from CG, GU, and GU posteradication patients. Target cells were HGC-27 cells treated with heat stress and patients’ sera. Effector cells were PBMCs stimulated with conA, H. pylori, and IL-12. The E/T ratio was 4. Specific cytotoxicity was only observed in GU patients’ lymphocytes.
