Lnc-C/EBPβ Modulates Differentiation of MDSCs Through Downregulating IL4i1 With C/EBPβ LIP and WDR5

• Published in: Frontiers in immunology Vol. 10; p. 1661
• Main Authors: Gao, Yunhuan, Shang, Wencong, Zhang, Dan, Zhang, Shiwu, Zhang, Xipeng, Zhang, Yuan, Yang, Rongcun
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 17.07.2019
• Subjects: H3K4me3; IL4il; Immunology; lncRNA; MDSC; WDR5; WDR5; MDSC; lncRNA; IL4il; H3K4me3
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2019.01661

Myeloid-derived suppressor cells (MDSCs), which play an important role in tumor and inflammatory diseases, are divided into two subsets CD11b Ly6C Ly6G monocytic MDSC (Mo-MDSC) and CD11b Ly6C Ly6G polymorphonuclear MDSC (PMN-MDSC) with different immunosuppressive function. However, it is poorly understood the mechanism(s) to control differentiation of Mo-MDSCs and PMN-MDSCs. Here, we found that β may promote PMN-MDSC but impede differentiation of Mo-MDSCs and . We demonstrated that β mediated differentiation of MDSCs was through downregulating multiple transcripts such as IL4il. β not only bound to C/EBPβ isoform LIP to inhibit the activation of C/EBPβ but also interacted with WDR5 to interrupt the enrichment of H3K4me3 mark on the promoter region of IL4i1. Data also imply that conserved homo β has a similar function with mouse β. Since MDSC subsets exert different suppressive function, β may be acted as a potential therapeutic target for inflammatory and tumor-associated diseases.