Molecular Mimicry between Helicobacter pylori Antigens and H⁺, K⁺-Adenosine Triphosphatase in Human Gastric Autoimmunity

Speaker: 萬書彣

Commentator: 許博翔 醫師

Time: 13:00-14:00 03/17/2004

Place: Room 601

Abstract

Autoimmune chronic gastritis (AIG) is an organ-specific inflammatory disease leading to hypochloridria and gastric atrophy and eventually pernicious anemia. AIG is characterized by lymphocytic infiltrates in the gastric mucosa and by destruction of parietal cells, resulting in mucosal atrophy¹. Gastric H⁺, K⁺-adenosine triphosphatase (ATPase) was identified as the autoantigen in both autoimmune gastritis and Helicobacter pylori-associated gastric atrophy². In this study, the authors identified the H⁺, K⁺-ATPase epitopes recognized by gastirc T-cell clones from four chronic AIG patients with current H. pylori infection and analyzed the TCR Vbchain repertoire of gastric T-cell clones. Furthermore, they screened the H⁺, K⁺-ATPase peptides and predicted the candidate cross-reactive H. pylori peptides. Gastric T-cell clones were tested for their proliferation and production of T helper type 1 cytokines stimulated by H⁺, K⁺-ATPase and H. pylori cross-reactive peptides. Addition in culture of anti-HLA-DR, but not anti-HLA-DQ, resulted in abrogation of the proliferation of T-cell clones. Taken together, cross-reactive T-cell clones may represent a significant component of the T cell response at AIG and the concomitant H. pylori infection.

References:

1.    Amedei, A., et al. (2003). Molecular mimicry between Helicobacter pylori antigens and H⁺, K⁺-adenosine triphosphatase in human gastric autoimmunity. J. Exp. Med. 198, 1147-1156.

2.    Bergman, M. P., et al. (2003). Characterization of H⁺, K⁺-ATPase T cell epitopes in human autoimmune gastritis. Eur. J. Immuol. 33, 539-545.