Abstract
ABSTRACT
Psoriasis is a common immune‐mediated inflammatory disease that often worsens during cold weather, yet the mechanisms linking cold exposure to enhanced psoriatic inflammation remain poorly understood. Shuai and colleagues identify a distinct macrophage population induced by cold stress in the dermal adipose layer, characterized by heightened lipid metabolism and IL‐1β production. These macrophages promote IL‐17A‐producing γδT‐cell responses in a mouse model of psoriasis, uncovering a potential cellular mechanism through which cold environments exacerbate psoriatic inflammation via immune‐metabolic pathways.