Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with genetic susceptibility and immune dysregulation. CARD11, a scaffolding protein in the CARD11-BCL10-MALT1 (CBM) complex, plays a central role in lymphocyte antigen receptor signaling. Recent studies have identified that various CARD11 mutations disrupt the development and function of regulatory T cells (Tregs), leading to a breakdown in immune tolerance that drives AD. This review summarizes the biological basis of CARD11, the clinical syndromes associated with its mutations, and the specific mechanisms of Treg dysfunction in AD, providing insights for targeted therapeutic strategies.

Key words: CARD11, atopic dermatitis, regulatory T cells, signal transduction