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Inflammation is the main mechanism of diseases caused by microbial, autoimmune, metabolic, and physical factors. In fact, we estimate that approx. 80% of all major human diseases, including heart attacks, strokes, sepsis, and early cancer, are mediated by inflammation. Proinflammatory cues are sensed by pattern recognition receptors such as Toll-like Receptors (TLRs) that are mainstays of innate immunity. These receptors generate signals that are transduced to the nucleus by an intricate network of intracellular adaptors. We study two families of these adaptors as potential targets for anti-inflammatory therapy to prevent reprogramming of the genome toward proinflammatory phenotype.
The first family of innate immunity adaptors of intense interest is MyD88 (myeloid differentiation 88) protein and its four relatives, including MAL, TRIF and SARM. We study them by identifying their cross-talk with TLRs and with each other. For example, we identified the RDR motif in Box 2 of MyD88 TIR domain as the interactive site with some members of TLR superfamily. This site is mutated in inborn errors of innate immunity characterized by pyogenic infections. We also unraveled a new function for another adaptor SARM.
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论文共 252 篇作者统计合作学者相似作者
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Manuel Chiusa,Youngmin A Lee,Ming-Zhi Zhang,Raymond C Harris,Taylor Sherrill, Volkhard Lindner,Craig R Brooks, Gang Yu,Agnes B Fogo,Charles R Flynn,Jozef Zienkiewicz,Jacek Hawiger,
Journal of Clinical Investigationno. 6 (2024)
Skin Health and Disease (2024)
Molecular Therapyno. 5 (2024): 1181-1184
Manuel Chiusa,Youngmin A. Lee,Ming-Zhi Zhang,Raymond C. Harris, Taylor Sherrill, Volkhard Lindner,Craig R. Brooks,Gang Yu,Agnes B. Fogo, Charles R. Flynn,Jozef Zienkiewicz,Jacek Hawiger,
JOURNAL OF CLINICAL INVESTIGATIONno. 6 (2024)
Scientific reportsno. 1 (2021): 11907-11907
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