Immune reactions against elongation factor 2 kinase: Specific pathogenesis of gastric ulcer from helicobacter pylori infection

Kiyoshi Ayada, Kenji Yokota, Yoshiro Kawahara, Yumiko Yamamoto, Kazuyuki Hirai, Tomoki Inaba, Masahide Kita, Hiroyuki Okada, Kazuhide Yamamoto, Keiji Oguma

Research output: Contribution to journalArticle

2 Citations (Scopus)


Helicobacter pylori (H. pylori) infection is a definite causative factor for gastric ulcers (GUs). In the present study we detected a specific antigen of gastric epithelial cells (HGC-27) using cell ELISA, which was recognized by the sera of GU patients (n = 20) but not in patients with chronic gastritis (CG; n = 20) or in healthy volunteers (HC; n = 10). This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes) from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1) and cytotoxic T lymphocyte (CTL) as opposed to those from CG patients. The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU.

Original languageEnglish
Article number850623
JournalClinical and Developmental Immunology
Publication statusPublished - 2009


ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Medicine(all)

Cite this