TPL2 mediates autoimmune inflammation through activation of the TAK1 axis of IL-17 signaling
Copyright policy )TPL2 mediates autoimmune inflammation through activation of the TAK1 axis of IL-17 signaling
Development of autoimmune diseases, such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), involves the inflammatory action of Th1 and Th17 cells, but the underlying signaling mechanism is incompletely understood. We show that the kinase TPL2 is a crucial mediator of EAE and is required for the pathological action of Th17 cells. TPL2 serves as a master kinase mediating the activation of multiple downstream pathways stimulated by the Th17 signature cytokine IL-17. TPL2 acts by linking the IL-17 receptor signal to the activation of TAK1, which involves a dynamic mechanism of TPL2–TAK1 interaction and TPL2-mediated phosphorylation and catalytic activation of TAK1. These results suggest that TPL2 mediates TAK1 axis of IL-17 signaling, thereby promoting autoimmune neuroinflammation.
- The University of Texas at Austin United States
- The University of Texas System United States
- The University of Texas MD Anderson Cancer Center United States
Central Nervous System, Inflammation, Mice, Knockout, Encephalomyelitis, Autoimmune, Experimental, Hematopoietic System, Interleukin-17, Autoimmunity, Cell Differentiation, Lymphocyte Activation, MAP Kinase Kinase Kinases, Radiation Tolerance, Article, Cell Line, Enzyme Activation, Gene Expression Regulation, Proto-Oncogene Proteins, Animals, Humans, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Protein Binding
Central Nervous System, Inflammation, Mice, Knockout, Encephalomyelitis, Autoimmune, Experimental, Hematopoietic System, Interleukin-17, Autoimmunity, Cell Differentiation, Lymphocyte Activation, MAP Kinase Kinase Kinases, Radiation Tolerance, Article, Cell Line, Enzyme Activation, Gene Expression Regulation, Proto-Oncogene Proteins, Animals, Humans, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Protein Binding
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