IL-35 Restricts Serine Metabolism to Suppress Effector T Cell Function in Atopic Dermatitis

Abstract IL-35 is an immunosuppressive cytokine and a critical regulator of immunity in autoimmune diseases. However, whether controls metabolism to inhibit T cell development atopic dermatitis (AD) remains unclear. In this study, we demonstrated that ameliorates AD by inhibiting the serine metabolic enzyme, phosphoserine aminotransferase 1 (PSAT1), mice humans. When major pathway was assessed, found increased activated cells. Measure ear thickness, histological examination showed treatment with inhibited inflammation suppressing expansion Th1, Th2, Th17 cells while inducing Foxp3-expressing Tregs. also regulated alterations glycolytic patients AD. Importantly, IL-35-mediated suppression Th2 amelioration correlated inhibition pathways, such as PSAT1, skin. Herein, effector directly regulating PSAT1. Therefore, therapies target serine-dependent pathways via could serve effective therapeutic strategies for