Here, we show that PsA-D effectively attenuated NiSO4-induced upregulation of DC activation markers CD54 and CD86, both in isolated DDC surrogates and in our full-thickness DDC-skin model, suggesting that PsA-D can modulate early immune activation, a crucial step in ACD pathogenesis. The gene discussed is CD86; the disease is granular corneal dystrophy type II.