Title: pp2ac/strn4 negatively regulates sting-type i interferon signaling in tumor associated macrophages authors: winson s. ho , isha mondal , beisi xu , oishika das , raymond sun , pochin chiou , xiaomin cai , foozhan tahmasebinia , caren yu-ju wu , zhihao wu , william matsui , michael lim , zhipeng meng , rongze olivia lu

HIGHLIGHTS

SUMMARY

Both tumor cells and myeloid cells express cGAS/STING, but accumulating evidence suggests that cGAMP is primarily produced by tumor cells and released as an immunotransmitter to activate STING in myeloid cells and stimulate antitumor immunity by triggering Type I IFN production(6-8). TAMs can promote immunosuppression and inhibit anti-tumor T_cell responses, thereby limiting the efficacy of checkpoint inhibitors(15-18). Mice with PP2Ac deficiency in macrophages exhibited reduced tumor growth, increased tumor-infiltrating 3 CD8+ T_cell and reduction of immunosuppressive macrophages. PP2Ac negatively regulates STING-Type I IFN signaling pathway To . . .

 



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