Related Experiment Videos

Increased PD-1 expression on CD4+ and CD8+ T cells is involved in immune evasion in gastric cancer

Hiroaki Saito1, Hirohiko Kuroda, Tomoyuki Matsunaga

  • 1Division of Surgical Oncology, Department of Surgery, Tottori University School of Medicine, Yonago, Japan. sai10@med.tottori-u.ac.jp

Abstract

Insights

Increased programmed death-1 (PD-1) on T cells correlates with immune evasion in gastric cancer. This suggests PD-1 upregulation on CD4+ and CD8+ T cells contributes to the disease.

Area of Science:

  • Immunology
  • Oncology

Background:

  • Co-signaling molecules are crucial for T cell function.
  • Programmed death-1 (PD-1) is an inhibitory receptor implicated in cancer immune evasion.
  • Elevated PD-1 on T cells is observed in various cancers.

Purpose of the Study:

  • To investigate PD-1 expression on T cells in gastric cancer patients.
  • To determine the relationship between PD-1 expression and immune evasion in gastric cancer.

Main Methods:

  • Analyzed PD-1 expression on CD4+ and CD8+ T cells using multicolor flow cytometry.
  • Samples included peripheral blood mononuclear cells (PBMC), normal gastric mucosa, and gastric cancer tissue.
  • Compared PD-1 expression between gastric cancer patients and healthy controls.

Main Results:

  • PD-1 expression was significantly higher on CD4+ and CD8+ T cells in gastric cancer patients compared to controls.
  • Elevated PD-1 levels correlated with disease progression.
  • Gastric cancer tissue showed higher PD-1 expression than normal mucosa and PBMC.
  • PD-1 positive T cells produced less Interferon-gamma (IFN-γ) than PD-1 negative T cells.

Conclusions:

  • Upregulation of PD-1 on both CD4+ and CD8+ T cells may contribute to immune evasion in gastric cancer.
  • PD-1 expression serves as a potential biomarker for immune evasion in gastric cancer.

Related Concept Videos

Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...