IL-17 signaling is regulated through intrinsic stability control of mRNA during inflammation

Differential IL-1β secretion by monocyte subsets is regulated by Hsp27 through modulating mRNA stability

Monocytes play a central role in regulating inflammation in response to infection or injury, and during auto-inflammatory diseases. Human blood contains classical, intermediate and non-classical monocyte subsets that each express characteristic patterns of cell surface CD16 and CD14; each subset also has specific functional properties, but the mechanisms underlying many of their distinctive fea...

IL-17 receptor signaling is required to control polymicrobial sepsis

Sepsis is a systemic inflammatory response resulting from the inability of the host to contain the infection locally. Previously, we demonstrated that during severe sepsis there is a marked failure of neutrophil migration to the infection site, which contributes to dissemination of infection, resulting in high mortality. IL-17 plays an important role in neutrophil recruitment. Herein, we invest...

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 ...

IL-17 enhances chemokine gene expression through mRNA stabilization.

IL-17 plays an important role in host defense and autoimmunity via the induction of proinflammatory gene expression, particularly in combination with TNF-alpha. The molecular mechanisms by which IL-17 regulates such expression are not well understood. Using the mouse chemokine CXCL1 (KC) gene as a model, we have examined the effects of IL-17 alone or in combination with TNF-alpha on transcripti...

Synergistic Effects on Endothelial Activation Recruitment during Inflammation through Sustain Neutrophil α IL-17 and TNF-