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Surface Antigen Profiling of Helicobacter pylori-Infected and -Uninfected Gastric Cancer Cells Using Antibody Microarray. | LitMetric

AI Article Synopsis

  • This study investigates the differences in CD antigen expression in gastric adenocarcinoma between patients infected and uninfected with Helicobacter pylori using the DotScan(™) antibody microarray, which screens 144 CD antibodies for a more comprehensive analysis than traditional methods.
  • Results revealed that cancer cells have higher CD antigen expression that helps them evade immune response, while specific H. pylori strains affect the expression of these antigens differently, influencing immune cell tolerance.
  • The findings highlight the complexity of immune interactions in gastric cancer and suggest that various H. pylori strains may exploit different mechanisms to modulate immune responses, potentially impacting treatment strategies.

Article Abstract

Background: Comprehensive immunophenotyping cluster of differentiation (CD) antigens in gastric adenocarcinoma, specifically between Helicobacter pylori-infected and -uninfected gastric cancer patients by using DotScan(™) antibody microarray has not been conducted. Current immunophenotyping techniques include flow cytometry and immunohistochemistry are limited to the use of few antibodies for parallel examination. We used DotScan(™) antibody microarray consisting 144 CD antibodies to determine the distribution of CD antigens in gastric adenocarcinoma cells and to elucidate the effect of H. pylori infection toward CD antigen expression in gastric cancer.

Methods: Mixed leukocytes population derived from gastric adenocarcinoma patients were immunophenotyped using DotScan(™) antibody microarray. AGS cells were infected with H. pylori strains and cells were captured on DotScan(™) slides.

Results: Cluster of differentiation antigens involved in perpetuating the tolerance of immune cells to tumor cells was upregulated in gastric adenocarcinoma cells compared to normal cells. CD279 which is essential in T cells apoptosis was found to be upregulated in normal cells. Remarkably, H. pylori-infected gastric cancer patients exhibited upregulated expression of CD27 that important in maintenance of T cells. Infection of cagA+ H. pylori with AGS cells increased CD antigens expression which involved in cancer stem cell while cagA- H. pylori polarized AGS cells to express immune-regulatory CD antigens. Increased CD antigens expression in AGS cells infected with cagA+ H. pylori were also detected in H. pylori-infected gastric cancer patients.

Conclusion: This study suggests the tolerance of immune system toward tumor cells in gastric cancer and distinct mechanisms of immune responses exploited by different H. pylori strains.

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Source
http://dx.doi.org/10.1111/hel.12295DOI Listing

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