Decreased Protein Kinase C-β Type II Associated with the Prominent Endotoxin Exhaustion in the Macrophage of FcGRIIb−/− Lupus Prone Mice is Revealed by Phosphoproteomic Analysis

摘要: Dysfunction of FcGRIIb, the only inhibitory receptor FcGR family, is commonly found in Asian population and possibly responsible for extreme endotoxin exhaustion lupus. Here, mechanisms prominent (LPS) tolerance FcGRIIb−/− mice were explored on bone marrow-derived macrophages using phosphoproteomic analysis. As such, LPS decreased several phosphoproteins macrophage, including protein kinase C-β type II (PRKCB), which was associated with phagocytosis function. Overexpression PRKCB attenuated RAW264.7 cells, supporting role this gene tolerance. In parallel, by phorbol 12-myristate 13-acetate (PMA) administration. This treatment induced C families, PRKCB. However, PMA severity cecal ligation puncture preconditioning but not wild-type cells. The significant reduction macrophage over cell more severe LPS-exhaustion increased infection susceptibility mice. PRKCB, improved LPS-tolerance, sepsis severity, predominantly enhancement might be a promising strategy to improve functions lupus patients LPS-tolerance from chronic infection.