Investigation of IL-23/Th17 axis in pathogenesis of psoriasis using a mouse model.

采用K5.Stat3C转基因小鼠作为银屑病模型，研究IL-23和IL-22在银屑病发病机制中的作用。K5Stat3C小鼠的银屑病样皮损的发展受到抑制，IL-23的产生不足。在另一只手中，IL-22缺陷小鼠产生的皮损与对照组小鼠相同。结果表明，IL-23在银屑病发病中起重要作用，在银屑病样皮损的发生发展过程中，一些替代途径可以弥补IL-22的丢失。

The roles of IL-23 and IL-22 in pathogenesis of psoriasis were investigated using K5.Stat3C transgenic mice, as a unique mouse model for psoriasis. The development of psoriasis-like lesions was attenuated in the K5.Stat3C mice being deficient in IL-23 production. In other hands, the lesions in the IL-22 deficient mice were generated as same as in the control mice. The results indicated that IL-23 played a significant role in psoriasis and that some alternative pathways could compensate the loss of IL-22 in development of psoriasis-like lesions.