Immune cell involvement in ulcer repair in radiation esophagitis and its role in the TGF‑β1/p38MAPK/FN axis (Review)

The present review explored the mechanism of the TGF-β1/p38MAPK/fibronectin (FN) signaling axis and immune cells during radiation esophagitis (RE) ulcer repair. A comprehensive analysis of the literature revealed that the TGF-β1/p38MAPK/FN signaling axis has a dual role in RE. Specifically, it initially promotes esophageal epithelial mucosal repair, but hyperactivation would then trigger tissue fibrosis. The intricate interplay between immune cells (macrophages, T cells and dendritic cells) and this signaling axis during the repair process of RE has been elucidated. Macrophages, in particular, serve a pivotal role in repair through polarization state switching. The influence of T-cell subpopulation differentiation and functional regulation on the immune response and tissue repair has also been demonstrated. By contrast, dendritic cells have been found to activate the immune response, though their function is repressed by TGF-β1. The complexity of RE's pathological process limits understanding into how the TGF-β1/p38MAPK/FN signaling axis precisely regulates immune cells at different repair stages, along with immune cells' properties and interactions. In the future, it is recommended that in-depth studies be conducted with the application of multi-omics and single-cell sequencing technologies, which are expected to contribute to the development of novel therapeutic strategies for RE and the advancement of RE clinical treatments.