Shizuo akira biography template
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Unc93 homolog B1 restricts systemic lethal inflammation by orchestrating TLR7 and TLR9 response
- Poster presentation
- Open access
- Published:
- Ryutaro Fukui1,
- Shin-Ichiroh Saitoh1,
- Atsuo Kanno1,
- Masahiro Onji1,
- Takuma Shibata1,2,
- Akihiko Ito4,
- Morikazu Onji5,
- Mitsuru Matsumoto6,
- Shizuo Akira7,8,
- Nobuaki Yoshida3 &
- …
- Kensuke Miyake1,2
Arthritis Research & Therapyvolume 14, Article number: P18 (2012) Cite this article
Nucleotide sensing-TLRs (Toll-like receptors) recognize pathogen derived-nucleic acids and trigger immune response [1]. Because of the highly conserved structure of nucleic acids, these TLRs have risk to recognize host derived-nucleic acids and induce autoimmune disease, therefore it is important to clarify the mechanisms and control the response.
We found that the responses of TLR7 and TLR9 are balanced reciprocally, and Unc93 homolog B1 (Unc93B1) is a key molecule for this balancing system [2]. Unc93B1
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CINBIO SEMINAR PROGRAMME
Na Sala dem Seminarios da Torre CACTI
- 10.00-10.45 Dr. Shizuo Akira - Osaka University
Conference Title: “Regnase-1, an endoribonuclease involved in inflammation, immunity and metabolism”
Abstract :
Regnase-1 fryst vatten an endoribonuclease involved in destabilization of a variety of mRNAs including IL-6 and Regnase-1 itself mRNAs. Regnase-1 knockout mice show generalized inflammation. Rengase-1 fryst vatten phosphorylated bygd a variety of stimuli. We generated a variety of tissue-specific KO mice and phosphorylation-resistant knock-in mice. I will talk about the role of Regnase-1 in a variety of cells and tissues.
- 11.00-11.45 Dr. Gabriel Núñez - University of Michigan Medical School
Conference Title: “Host-Microbiota Interactions in Health and Disease”
Abstract:
The intestinal tract of mammals fryst vatten colonized bygd a large number of microorganisms that are referred to collectively as the gut microbiota. The seminar will focus on research perform
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Abstract
Periodontitis, which is induced by repeated bacterial invasion and the ensuing immune reactions that follow, is the leading cause of tooth loss. Periodontal tissue is comprised of four different components, each with potential role in pathogenesis, however, most studies on immune responses focus on gingival tissue. Here, we present a modified ligature-induced periodontitis model in male mice to analyze the pathogenesis, which captures the complexity of periodontal tissue. We find that the inflammatory response in the peri-root tissues and the expression of IL-6 and RANKL by Thy-1.2− fibroblasts/stromal cells are prominent throughout the bone destruction phase, and present already at an early stage. The initiation phase is characterized by high levels of ST2 (encoded by Il1rl1) expression in the peri-root tissue, suggesting that the IL-33/ST2 axis is involved in the pathogenesis. Both Il1rl1- and Il33-deficient mice exhibit exacerbated bone loss in the acute phase o