GSE212010
ERMAP improves inflammatory bowel disease by regulating macrophage and T cell functions
Background & aims: Both macrophages and T cells play a critical role in inflammatory bowel disease (IBD) development. Since our previous studies have shown that a novel immune checkpoint molecule ERMAP affects macrophage polarization and negatively regulate T cell responses, we investigated the effects of ERMAP on IBD progression in mice. Methods: Using an dextran sodium sulfate (DSS)-induced IBD mice model, knockdown of ERMAP in RAW264.7 macrophages, ERMAP gene knockout mice, and Global gene expression analysis by RNA-seq, We investigate the effect of ERMAP on IBD by regulation of T cells and macrophages, NOD-like receptor (NLR) protein family pathway in macrophages. Results: We show here that administration of ERMAP protein significantly increases the proportion of anti-inflammatory M2-type macrophages and inhibits T cell activation and proliferation in IBD mice induced by DSS. Knockdown of ERMAP in RAW264.7 macrophages reduces M2-type macrophage polarization and increases T cell responses. Adoptive transfer of macrophages from ERMAP knockout mice exacerbates DSS-induced IBD. Global gene expression analysis by RNA-seq shows that ERMAP inhibits the NLR protein family pathway in macrophages. Conclusions: Our results suggest that ERMAP protein has the potential to be used in the treatment of IBD by regulating macrophage and T cell functions. Overall design: Comparison of differential genes in RAW264.7 after knockdown of ERMAP by RNA-seq