
IndraLab
Statements
reach
"While IL-1R1 can be stimulated by either of two cytokines, IL-1alpha or IL-1beta, it has been shown that IL-1beta plays a pivotal role in disease pathogenesis because it not only directly stimulates IL-1R1-dependent inflammatory signaling, but is also needed for the secretion of IL-1alpha from cells."
reach
"A major branch of the innate immune system is regulated by the Toll like receptors (TLRs), which are receptors for endogenous damage associated molecules released from injured cells as well as pathogen derived molecules, and interleukin-1 receptors (IL-1R), which are activated by IL-1alpha, IL-1beta and IL-18 cytokines."
reach
"Because of the intermediate role of IRAK-1 in the activation of NF-kappaB after IL-1R stimulation by IL-1alpha,, we examined the correlation between the immunohistochemical expression of IRAK-1 with that of IL-1 alpha (an IL- 1R ligand) and NF-kappaB using the 306 NSCLCs placed in TMAs."
reach
"These include CXCL1/KC and probably CXCL2, 5, and 8, which recruit neutrophils from limbal capillaries to the corneal stroma, and IL-1alpha and IL-1beta, which then feedback to activate the IL-1R1 and MyD88 pathway in macrophages and most likely also in resident corneal epithelial cells and stromal fibroblasts."
reach
"We also show that P. aeruginosa activates NF-kappaB in macrophages through both the TIR containing adaptor protein (TIRAP)/MyD88 dependent and the TRIF dependent pathways, and that IL-1alpha and IL-1beta activation of IL-1R1 is an important feedback pathway in the host response to P. aeruginosa."
sparser
"We also show that P. aeruginosa activates NF-κB in macrophages through both the TIR-containing adaptor protein (TIRAP)/MyD88 dependent and the TRIF-dependent pathways, and that IL-1α and IL-1β activation of IL-1R1 is an important feedback pathway in the host response to P. aeruginosa."
sparser
"Following EGFR activation IL-1α is released and activates IL-1R on keratinocytes creating a second autocrine loop leading to the activation of NF-κB signaling that modifies expression of specific keratinocyte genes involved in tumor formation including increasing expression and release of CXC ligands such as CXCL1 ( xref )."