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High Levels of Class I Major Histocompatibility Complex mRNA Are Present in Epstein-Barr Virus-Associated Gastric

Farhad Ghasemi1, Steven F Gameiro2, Tanner M Tessier2

  • 1Department of Surgery, Western University, London, ON N6A 3K7, Canada.

Cells
|February 27, 2020
PubMed

Insights

Epstein-Barr virus (EBV) does not reduce major histocompatibility complex I (MHC-I) in most stomach cancers. Instead, EBV-associated gastric cancers show higher MHC-I mRNA levels, suggesting a different immune response mechanism.

Area of Science:

  • Oncology
  • Virology
  • Immunology

Background:

  • Epstein-Barr virus (EBV) is linked to 9% of stomach adenocarcinomas.
  • EBV microRNAs were previously thought to evade immune responses by reducing MHC-I antigen presentation.
  • This study investigates EBV's effect on the MHC-I pathway in gastric cancer.

Purpose of the Study:

  • To assess the impact of EBV on MHC-I heavy and light chain mRNA levels in human gastric carcinomas.
  • To investigate the relationship between EBV, MHC-I expression, and immune cell infiltration in gastric cancer.

Main Methods:

  • Analysis of mRNA levels for MHC-I components and antigen processing/presentation factors.
  • Utilized data from nearly 400 human gastric carcinomas (GCs).
  • Correlated gene expression with intratumoral interferon-gamma levels and immune cell infiltration.

Main Results:

  • Contrary to expectations, MHC-I mRNA levels were not reduced in EBV-associated gastric carcinomas (EBVaGCs).
  • MHC-I and related gene mRNA levels were as high or higher in EBVaGCs compared to normal tissues and other GC subtypes.
  • Upregulation correlated with increased interferon-gamma and T/NK cell infiltration in EBVaGCs.

Conclusions:

  • EBV-encoded products do not effectively reduce MHC-I antigen presentation machinery mRNA levels in human gastric cancer.
  • EBVaGCs exhibit an upregulation of MHC-I pathway components, potentially driven by interferon-gamma.
  • This suggests a complex interplay between EBV and the host immune response in gastric carcinogenesis.
Keywords:
EBVEBVaGCEpstein–Barr virusMHC-ITCGAantigen presentationimmune evasionmajor histocompatibility complexstomach adenocarcinoma

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