SETD1B Activates iNOS Expression in Myeloid-Derived Suppressor Cells.

ABSTRACT: Inducible nitric oxide synthase (iNOS) generates nitric oxide (NO) in myeloid cells that acts as a defense mechanism to suppress invading microorganisms or neoplastic cells. In tumor-bearing mice, elevated iNOS expression is a hallmark of myeloid-derived suppressor cells (MDSC). MDSCs use NO to nitrate both the T-cell receptor and STAT1, thus inhibiting T-cell activation and the antitumor immune response. The molecular mechanisms underlying iNOS expression and regulation in tumor-induced MDSCs are unknown. We report here that deficiency in IRF8 results in diminished iNOS expression in both mature CD11b⁺Gr1^- and immature CD11b⁺Gr1⁺ myeloid cells in vivo Strikingly, although IRF8 was silenced in tumor-induced MDSCs, iNOS expression was signi

SUBMITTER: Redd PS 

PROVIDER: S-EPMC5495112 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature