Abstract
Posttranslational modifications (PTMs) of proteins, particularly acetylation, phosphorylation, and ubiquitination, play critical roles in the host innate immune response. PTMs’ dynamic changes and the crosstalk among them are complicated. To build a comprehensive dynamic network of inflammation-related proteins, we integrated data from the whole-cell proteome (WCP), acetylome, phosphoproteome, and ubiquitinome of human and mouse macrophages. Our datasets of acetylation, phosphorylation, and ubiquitination sites helped identify PTM crosstalk within and across proteins involved in the inflammatory response. Stimulation of macrophages by lipopolysaccharide (LPS) resulted in both degradative and non-degradative ubiquitination. Moreover, this study contributes to the interpretation of the roles of known inflammatory molecules and the discovery of novel inflammatory proteins.
Highlights
Macrophages are resident phagocytic cells which act as effector cells in innate immune system and play a crucial role in initiating adaptive immunity by means of recruiting other immune cells [1]
Existing research recognizes the critical role of the phosphorylation of innate immune adaptor proteins
The phosphorylation of MAVS, STING, and TRIF is necessary for interferon regulatory factor 3 (IRF3)’s recruitment and type I IFN’s production, which is essential for the activation of antiviral immunity [6]
Summary
Macrophages are resident phagocytic cells which act as effector cells in innate immune system and play a crucial role in initiating adaptive immunity by means of recruiting other immune cells [1]. Located throughout the tissues in the body, macrophages are among the first defensive cells to interact with foreign or abnormal host cells and their products They are the most efficient phagocytes that can ingest and process foreign materials, dead cells and debris; they release various secretory products to mobilize other host cells and influence other resident cells in the inflammatory response [2]. Phosphorylation is a widely investigated type of PTM in innate immunity [4]. It is catalysed by protein kinases and reversed by protein phosphatases. The phosphorylation of MAVS, STING, and TRIF is necessary for IRF3’s recruitment and type I IFN’s production, which is essential for the activation of antiviral immunity [6]
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