Immune Cells Stuck in Inflammatory State May Explain Chronic Diabetic Wounds
A review by Yi Ru and colleagues examined how many immune cell types behave during wound healing and how diabetes disrupts those patterns. In diabetic wounds, macrophages may remain in pro-inflammatory states instead of shifting toward repair, prolonging damage and blocking healing. The findings suggest reprogramming immune responses could lead to more targeted treatments for diabetic ulcers.
The review by Yi Ru and colleagues surveyed multiple immune cell populations, including monocytes, macrophages, dendritic cells, neutrophils, mast cells, B cells, T cells, and natural killer cells. It tracked where these cells appear during healing stages and how diabetes alters their timing and behavior.
In normal repair, monocytes enter injured tissue and become macrophages that shift from inflammatory M1-like states to reparative M2-like states. Diabetic wounds can disrupt this switch. Poorly controlled neutrophil extracellular traps, altered mast cell degranulation, and impaired dendritic cell clearance of apoptotic cells may sustain inflammation and delay repair.
If these immune-cell insights translate into treatments, people with diabetes who develop chronic ulcers could benefit from therapies aimed at shifting macrophages and other cells toward repair. That may reduce suffering, amputation risk, and caregiving burdens. Health systems might also face lower long-term costs, though any clinical benefit would depend on further research and accessible delivery.