Growing evidence are showing a pivotal role of macrophages (M) and microglia (MG) in the pathogenesis of Multiple sclerosis (MS). Interferon  (IFN ) and glucocorticoids are front line treatments in MS, and disrupting either type I IFN or GC receptor (GR) pathway in mice aggravates EAE, the mouse model of MS. Here, we evaluated GR Interacting Protein 1 actions in neuroinflammation by subjecting mice conditionally lacking GRIP1 in myeloid cells (cKO) to EAE. We showed that myeloid GRIP1 plays a dual role by promoting the effector neuroinflammatory phase of EAE as well as mediating IFN  therapeutic effect. Our sorted M/MG transcriptome analysis reveals dramatic changes in inflammatory and IFN-pathway gene expression including potential differences of GRIP1 function in these distinct myeloid cell populations. SOURCE: Yurii ChinenovHSS Genomics Center Hospital for special surgery

Pluto Bioinformatics

GSE141721: Transcriptionnal coregulator GRIP1 differentially modulate myeloid cell-driven neuroinflammation and response to IFN-beta therapy