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Increased programmed death-ligand-1 expression in human gastric epithelial cells in<i>Helicobacter pylori</i>infection

2010/07/14 by Y-Y Wu, C-W Lin, K-S Cheng +8
Medicine · #Clostridium difficile and Clostridium perfringens research #Gastrointestinal disorders and treatments #Helicobacter pylori-related gastroenterology studies

paper · pdf · doi:10.1111/j.1365-2249.2010.04217.x

crossref issued 2010/07/14 · crossref published 2010/07/14 · crossref published-online 2010/07/14 · openalex publication_date 2010/07/14 · crossref created 2010/07/14 · crossref published-print 2010/08/16 · openalex created_date 2016/06/24 · crossref deposited 2023/06/02 · crossref indexed 2026/07/28 · openalex updated_date 2026/08/01

Abstract

B7-H1 [programmed death-ligand-1 (PD-L1)] is a B7-family member that binds to programmed death-1 (PD-1). Recently, deficiency of PD-L1 has been demonstrated to result in accelerated gastric epithelial cell damage in gastritis, and PD-L1 is suggested to play a critical role in regulating T cell homeostasis. Here, we aimed to gain more insight into gastric PD-L1 expression, regulation and function during Helicobacter pylori infection. PD-L1 expression in human gastric epithelial cells was analysed using Western blotting, quantitative polymerase chain reaction and fluorescence activated cell sorter analysis. Furthermore, co-culture experiments of human gastric epithelial cells with primary human T cells or Jurkat T cells were conducted. PD-L1 expression in primary human gastric epithelial cells was strongly enhanced by H. pylori infection and activated T cells, and augmented markedly by further stimulation with interferon-γ or tumour necrosis factor-α. Moreover, PD-L1 expression in gastric epithelial cells significantly induced apoptosis of T cells. Our results indicate that a novel bidirectional interaction between human gastric epithelial cells and lymphocytes modulates PD-L1 expression in human gastric epithelial cells, contributing to the unique immunological properties of the stomach.

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