Environmental Low-Dose Radiation Activates Th1 Immunity through the Mitochondria-STING Pathway

Area of Science:

• Immunology
• Radiation Biology
• Cancer Research

Background:

• Environmental low-dose radiation (LDR) prevalence is increasing.
• The impact of LDR on the immune system is not well understood.

Purpose of the Study:

• To investigate the specific effects of LDR on immune cell populations.
• To elucidate the underlying molecular mechanisms of LDR-induced immune changes.
• To evaluate the potential of LDR in enhancing antitumor immunity.

Main Methods:

• In vitro and in vivo experiments using splenocytes and peripheral blood T cells.
• Mitochondrial damage assessment and STING signaling pathway analysis.
• Murine model of triple-negative breast cancer exposed to whole-body LDR.

Main Results:

• LDR selectively increased CD4+ IFNγ+ Th1 splenocytes and T cells without affecting CD8+ Tc1 or regulatory T cells.
• LDR-induced mitochondrial damage activated the STING pathway, upregulating T-bet and Th1 differentiation.
• LDR exposure delayed tumor growth, promoted cell death, and increased tumor-infiltrating Th1 cells and macrophages in a mouse cancer model.

Conclusions:

• Environmental LDR specifically modulates Th1 T-cell responses via the STING pathway.
• LDR demonstrates potential for enhancing antitumor immunity and warrants further investigation for clinical applications.