TGFB1 and acute respiratory distress syndrome: Th17 cells exert pro‐inflammatory effects primarily through Il‐17 secretion, while Treg cells counterbalance inflammation by releasing cytokines including IL‐10 and TGF‐β, thereby inhibiting Th17 responses.[9, 35, 36] Emerging evidence indicates that Tregs are vital for suppressing pulmonary inflammation and promoting tissue repair and regeneration.[11, 37] In patients, a higher Th17/Treg ratio in BALF is regarded as a negative prognostic factor for ARDS.[10] In this study, we propose that Ly6C+ cDC2 is a core mediator in balancing Th17 and Treg cells within the organism.