Immune Pathway Contributing to Radiation Therapy-Related Lung Damage Identified in Mice
Working with a mouse model of radiation-induced lung injury, researchers uncovered an immune pathway that may contribute to radiation-related lung damage and, suggest their results may point to a potential preventive strategy. The post Immune Pathway Contributing to Radiation Therapy-Related Lung Damage Identified in Mice appeared first on GEN - Genetic Engineering and Biotechnology News .
In a study published in Nature Communications, researchers from City of Hope have identified an immune pathway that contributes to radiation therapy-related lung damage in mice. The findings, led by Dr. Heather McGee, could lead to new preventive strategies for radiation-induced lung injury (RILI), which affects up to 20% of lung cancer patients undergoing radiation therapy.
The researchers developed a mouse model of radiation-induced lung injury and focused on innate lymphoid cells (ILCs) as potential contributors to RILI. They found that radiation therapy transforms protective ILC2 cells into inflammatory ILC1 cells, promoting lung tissue damage. This transformation is driven by increased levels of the signaling protein interferon-beta (IFN-β), which acts as a switch from protective to inflammatory cell function.
Tests on human ILCs showed similar biological changes, suggesting the findings' relevance to humans. The researchers then tested whether blocking the IFN-β signaling pathway during radiation could prevent the harmful immune cell transformation. In mice, disrupting this pathway reduced inflammation, limited lung injury, and decreased fibrosis, a permanent lung scarring.
Lead author Dr. Jaeho Kim stated that their findings identify type I IFN-mediated ILC plasticity as a mechanism underlying RILI pathogenesis. Disrupting IFN-β signaling could potentially offer a treatment to reduce this debilitating side effect, expanding radiation options for patients with chronic lung conditions and enabling more aggressive radiation treatment when needed.
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