Shizuo Akira

TL;DR: It is shown that TLR4 and MyD88, but not Mal or TRIF, are essential for the control of exponential S. Typhimurium growth, suggesting thatTLR4 signalling is not important in driving bacterial clearance in comparison to its critical role in controlling early bacterial growth in mouse typhoid.

TL;DR: Results indicate that Stat3 functions as a negative regulator of G‐ CSF signaling by inducing SOCS3 expression and that ERK activation is the major factor responsible for inducing the proliferation of hematopoietic cells in response to G‐CSF.

TL;DR: Cisplatin-induced TLR4 expression and its binding to LPS in mouse cochlear tissues and the effect of this interaction on hearing function are investigated to suggest that hearing function can be easily damaged by increased TLR expression and microbial infections due to the weakened host defense systems of cancer patients receiving therapy.

TL;DR: It is established that TTSS1-dependent secretion and translocation of a V. parahaemolyticus effector protein VP1686 into the cytosol induces DNA fragmentation in macrophages, and an important role is suggested for Vibrio effectorproteinVP1686 that activate a conserved apoptotic pathway in Macrophages through suppression of NF-κB activation independent of Toll-like receptor signaling.

TL;DR: Combined stimulation of THP-1 cells with LPS and IFN-γ up-regulate mCD14, TLR4, MD-2 and MyD88 expression by these cells, which might be involved in synergistic IL-8 production by the cells.