1095 A2a regulates the polarization of M1 macrophages to initiate innate immunity in psoriasis

Background: Psoriasis is a common systemic inflammatory disease whose pathogenesis closely related to metabolism and immunity. Macrophages are the main sources of IL-23 TNF-a in innate immune, which play an important role initiation development psoriasis become new focus this field. However, it remains be explored how macrophage plasticity mediates immune response its regulatory mechanism. Objective:Our aim elucidate polarization look for switches that regulate psoriasis. Methods: Immunohistochemistry, Flow cytometry RT-pcr were defected infiltration. WT knockout mice analyzed inflammation with Imiquimod (IMQ) or rmIL23-induced mice. RNA-seq was used find signaling pathways. Si-RNA western blot verify pathway. Result: We conformed macrophages have increased infiltration lesions mouse lesions, psoriasis-like has been improved after depletion Clodronate Liposomes Further, we found A2a key M1 polarization. A2a-/-mice could enhance IMQ-induced through increasing Conversely, agonist CGS 21680 HCl significantly alleviate IMQ mrIL-23-induced decreasing Finally, Krt16 expressed on macrophages, never reported before regulates expression depending NF-KB pathway, knocking down inhibited. Conclusion: inhibits by downregulating pathway inhibit early Key words: Psoriasis, A2a, macrophage, NF-KB,