Yi Lu

TL;DR: The data show that Act1 is essential in IL-17-dependent signaling in autoimmune and inflammatory disease and was associated with much less inflammatory disease in vivo in both autoimmune encephalomyelitis and dextran sodium sulfate–induced colitis.

TL;DR: It is proposed that Act1 mediates IL- 17–induced signaling pathways through its E3 ubiquitin ligase activity and that TRAF6 is a critical substrate of Act1, which indicates the importance of protein ubiquitination in the IL-17–dependent inflammatory response.

TL;DR: It is found that SIGIRR formed a complex with ST2 upon IL-33 stimulation and specifically inhibited IL- 33/ST2-mediated signaling in cell culture model, suggesting an important role in the regulation of Th2 response in vivo.

TL;DR: The essential role of epithelial-derived Act1 is demonstrated for the understanding of pathobiology of atopic diseases, including allergic asthma, which identifies Act1 as a potential therapeutic target through the distinct impact of the IL-17R-Act1 and IL-25R- act1 axes.

TL;DR: Through the study of these IRAK modification mutants, two parallel IL-1-mediated signaling pathways for NFκB activation, TAK1-dependent and MEKK3-dependent, respectively are uncovered and provide significant insight to the further understanding of NFκBs activation pathways.