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Alcohol exposure significantly impairs T cell cytotoxicity and activation, contributing to liver damage in ALD.61 A marked decrease in C-C chemokine receptor type 5 (CCR5) expression on CD4 + T cells has been observed in patients with AH, which may disrupt the balance between pro-inflammatory Th1 cells and anti-inflammatory Th2 cells, leading to a more severe inflammatory response.64 Th17 cells, which produce IL-17, drive inflammation by recruiting neutrophils to the liver,65 further exacerbating inflammation and injury.66 Elevated IL-17 levels are commonly seen in patients with ALD, particularly in those with advanced diseases such as AH.66 67 Studies suggest that targeting and blocking the IL-17 pathway can reduce alcohol consumption and liver damage, highlighting IL-17 as a therapeutic target.67 Additionally, the imbalance between Tregs and Th17 cells is critical in ALD progression