Early iTreg administration effectively reversed these effects by suppressing proinflammatory cytokines, restoring IL-10 levels, reducing immune cell infiltration, and mitigating tissue damage.<h4>Conclusions</h4>These findings demonstrate that iTreg therapy effectively modulates the hyperinflammatory response in ALI and may represent a promising strategy for treating severe inflammatory lung diseases. This evidence concerns the gene IL10 and acute respiratory distress syndrome.