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Myeloid-derived suppressor cells (MDSCs), which play an important role in tumor and inflammatory diseases, are divided into two subsets CD11b + Ly6C hi Ly6G −  monocytic MDSC (Mo-MDSC) and CD11b + Ly6C low/neg 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  lnc-C/EBP β may promote PMN-MDSC but impede differentiation of Mo-MDSCs  in vitro  and  in vivo . We demonstrated that  lnc-C/EBP β mediated differentiation of MDSCs was through downregulating multiple transcripts such as IL4il.  Lnc-C/EBP 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  lnc-C/EBP β has a similar function with mouse  lnc-C/EBP β. Since MDSC subsets exert different suppressive function,  lnc-C/EBP β may be acted as a potential therapeutic target for inflammatory and tumor-associated diseases.

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