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CD103+ T Cells Eliminate Damaged Alveolar Epithelial Type II Cells Under Oxidative Stress to Prevent Lung

Yu Xu1, Haorui Luo1, Jiahao Wang1

  • 1Key Laboratory of Multicellular Systems, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|May 9, 2025
PubMed

Insights

Decline in CD103+ T cells, crucial for lung cancer prevention, leads to oxidative damage in epithelial cells and promotes tumor growth. Aged lungs show reduced CD103+ T cells, increasing lung adenocarcinoma risk.

Area of Science:

  • Immunology
  • Oncology
  • Aging Research

Background:

  • Aging is linked to immune system decline and increased cancer risk, but the mechanisms are unclear.
  • Lung adenocarcinoma can arise from alveolar epithelial type II (AT2) cells.
  • The role of specific T cell populations in preventing age-related lung tumorigenesis needs further investigation.

Purpose of the Study:

  • To investigate the link between T cell function, aging, and lung cancer development.
  • To determine the role of CD103+ T cells in preventing lung adenocarcinoma.
  • To explore the impact of Med23 depletion in T cells on lung tumorigenesis.

Main Methods:

  • Utilized a mouse model with Med23-depleted T cells (Med23-/-).
  • Analyzed T cell populations (CD103+ T cells) and AT2 cell status in mouse lungs.
  • Performed in vitro co-culture experiments to assess T cell killing capacity.
  • Examined aged animals for changes in CD103+ CD8+ T cells and AT2 cells.

Main Results:

  • Reduced CD103+ T cells in Med23-/- mice correlated with spontaneous lung adenocarcinomas originating from AT2 cells.
  • CD103+ T cells were found to eliminate AT2 cells with oxidative damage and suppress KRAS-driven tumorigenesis.
  • CD103+ CD8+ T cells demonstrated killing capacity proportional to target cell oxidative stress.
  • Aged mice exhibited decreased lung CD103+ CD8+ T cells and increased oxidative-damaged AT2 cells.

Conclusions:

  • CD103+ T cells are vital for immune surveillance of epithelial cells under oxidative stress, preventing lung cancer.
  • Age-related decline in CD103+ CD8+ T cells contributes to lung tumorigenesis through impaired elimination of damaged AT2 cells.
  • Impaired T cell immunity in aged lungs represents a potential driver of lung cancer development.
Keywords:
AT2 cellCD103+ T cellMED23lung adenocarcinomaoxidative stresstumorigenesis

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