The expression and function of the B7 family in Helicobacter pylori infection and gastric carcinogenesis process

Abstract

Gastric cancer (GC) was the fifth most common cancer and the fourth leading cause of cancer-related deaths worldwide in 2020. 1 In 2010-2014, the 5-year-survival was very high in Korea (69%) and Japan (60%), but in China, it was only 35.9%, 2 where initial asymptomatic development and subsequent nonspecific symptoms result in a diagnosis at advanced stages with a poor prognosis. Assuming that the current incidence rates remain the same, the annual number of new GC cases are predicted to increase from 1.09 million cases to 1.77 million cases by 2040. 3 Helicobacter pylori is an important GC risk factor. 4 The Correa model 5 demonstrates the progression of human gastric carcinogenesis from the normal gastric mucosa to cancer. Persistent H. pylori

Strategies of Helicobacter pylori in evading host innate and adaptive immunity: insights and prospects for therapeutic targeting

“…As early as 1998, in vivo studies had demonstrated that gastric epithelial cells (GECs) upregulate the expression of B7 costimulatory molecules (B7-1, B7-2, B7-H1, and B7-H2) during H. pylori infection. This upregulation helps diminish the activity of CD4+ effector T cells and increase Treg cells, thereby modulating the T cell response ( Ye et al., 1997 ; Zhang et al., 2023 ). B7-H2 (ICOS ligand), a recent addition to the B7 receptor family, provides a costimulatory signal upon binding with ICOS, enhancing T cell activity.…”