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STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 + T Helper Cell Differentiation in Non-Small Cell

Roshni Bibi1, Melvin George2, Koustav Sarkar1

  • 1Cancer Immunology and Gene Technology Lab, Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, India.

Immunology
|February 5, 2026
PubMed

Insights

STAT2 protein depletion in CD4+ T cells enhances anti-cancer immunity in non-small cell lung cancer (NSCLC). This approach reduces oxidative stress and boosts anti-tumour responses, offering a potential therapeutic strategy.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) requires novel therapies to improve anti-tumour immunity.
  • CD4+ T helper cells are critical for mounting an effective anti-cancer immune response.

Purpose of the Study:

  • To investigate the role of STAT2 protein in CD4+ T cells within the context of NSCLC.
  • To assess the impact of STAT2 ablation on T cell function and epigenetic modifications in NSCLC patients.

Main Methods:

  • CRISPR/Cas9 gene editing was used to deplete STAT2 in CD4+ T cells from stage I NSCLC patients (n=30).
  • Evaluated cellular functions, epigenetic pathways, cytokine production, and T cell activation.

Main Results:

  • STAT2 depletion significantly enhanced the anti-cancer efficacy of T lymphocytes.
  • Reduced oxidative stress and DNA methylation, while increasing beneficial TH1 cytokine synthesis.
  • STAT2-deficient T cells demonstrated improved activation of cytotoxic T lymphocytes against cancer cells.

Conclusions:

  • STAT2 is identified as a key regulator of immune function in the NSCLC microenvironment.
  • Targeted STAT2 inhibition in tumour-reactive T cells could restore anti-tumour immunity.
  • Further research is needed for systemic STAT2 inhibition strategies.
Keywords:
CD4+ T helper cellsCRISPR/Cas9 knock outDNA methylationRNA–DNA hybrid immunoprecipitation (RDIP)STAT2m6A RNA methylation

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