IL-22 downregulates Cx43 expression and decreases gap junctional intercellular communication by activating the JNK pathway in psoriasis

The roles of interleukin-22 (IL-22) in the pathomechanisms of psoriasis have been well demonstrated. Gap junctional intercellular communication (GJIC) is widely known for its involvement in multiple biological and pathological processes such as growth-related events, cell differentiation, and inflammation. Here, we show that IL-22 significantly decreased GJIC and downregulated Cx43 expression in HaCaT cells. Cx43 overexpression markedly inhibited the proliferation of and increased GJIC in HaCaT cells, while the silencing of Cx43 exerted the opposite effects.