Irf7, or Interferon Regulatory Factor 7, is a master transcriptional factor that plays a pivotal role in producing IFN-I and regulating the innate immune response. It is involved in multiple signaling pathways, including those related to IFN-I production at the signaling, transcription, translation, and post-translational levels. Additionally, it is important for dimerization, nuclear translocation, and has a role in IFN-III and COVID-19. IRF7 is mainly expressed in immune cells but also present in keratinocytes, fibroblasts, and dermal cell types, being crucial for skin immunity, inflammation, and fibrosis [1,4].

In sepsis-induced acute lung injury, specific inhibition of Irf7 significantly improved the symptoms. Irf7 transcriptionally activates Srg3, which promotes ferroptosis and M1 macrophage polarization via the NF-κB signaling pathway, exacerbating septic lung injury [2]. In Candida albicans infection, Irf7-/-mice showed stronger phagocytosis of the fungus, upregulated CD209 expression, and enhanced autophagic signaling in macrophages, indicating that IRF7 exacerbates the infection by compromising macrophage functions [3]. In osteosarcoma, IRF7 was downregulated, and higher expression correlated with better survival. It inhibited the Warburg effect by suppressing PKM2 transcription, suggesting its tumor-suppressive role [5].

In conclusion, Irf7 is essential for regulating the innate immune response, especially in IFN-I production. Model-based research, such as gene knockout (KO) in mice, has revealed its role in various disease conditions. In sepsis-induced acute lung injury, it exacerbates the condition, while in Candida albicans infection, it enhances the susceptibility. In osteosarcoma, it acts as a tumor suppressor. These findings contribute to our understanding of the biological functions of Irf7 and its potential as a therapeutic target in related diseases.