IL1B and psoriasis: Since these above cytokines are known to promote Th17 cell differentiation, we may speculate that in the pathological condition of psoriasis, the release of pro‐inflammation mediators of IL‐6, IL‐1β, and TNF‐α may in turn impose on microglia and local immune cells to produce IL‐17A, then further aggravate the neuroinflammation and depression development.