Based on the above results, we propose the mechanism of rhIL-23R-CHR/Fc in the treatment of psoriasis: On the one hand, rhIL-23R-CHR/Fc binds to free IL-23 to directly inhibit the differentiation of Th17 cells; on the other hand, rhIL-23R-CHR/Fc suppresses the activation of IL-22-secreting ILC3 cells and indirectly affects the pathogenesis of the disease through skin-intestinal interaction. This evidence concerns the gene IL22 and psoriasis.