Inflammatory monocyte-derived dendritic cells mediate autoimmunity in murine model of systemic lupus erythematosus.

ABSTRACT: Using a mouse model of systemic lupus erythematosus (SLE), we recently demonstrated that the two major manifestations of SLE are mechanistically independent because the type I IFN pathway leads to the autoantibody production whereas the NF-κB activation is sufficient for the development of glomerulonephritis. To further advance our understandings on the molecular pathways regulating the development of SLE, we studied the role of IRF8 because it controls both type I IFN and NF-κB pathways and saw that IRF8-deficient mice failed to develop either glomerulonephritis or the autoantibody production. Furthermore, these genetically engineered mice prompted us to realize the important role of Ly6C^high inflammatory monocytes in the development of SLE. These monocytes migrate to the perit

SUBMITTER: Miyagawa F 

PROVIDER: S-EPMC7388367 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature