机译:ILC3s与更高水平的增加IL 1小鼠β加剧炎症性关节炎缺乏吞噬NADPH氧化酶
Division of Organ TransplantationOsaka University. Graduate School of MedicineOsaka,Japan;
Division of Rheumatology, Immunology, and AllergyBrigham and Women's HospitalBoston,MA,USA;
National Laboratory Animal CenterNational Applied Research LaboratoriesTainan,TaiwanInstitute of Clinical MedicineNational Cheng‐Kung University Medical CollegeTainan,Taiwan;
Granulomatous Disease, Chronic, X-Linked; DUOX2 gene; NADPH OxidaseCYBB geneLymphoid CellsArthritisReactive Oxygen SpeciesInflamed joint;
机译:!CDATAVariations of Emphasis Type="SmallCaps"l/Emphasis- and Emphasis Type="SmallCaps"d/Emphasis-amino acid levels in the brain of wild-type and mutant mice lacking Emphasis Type="SmallCaps"d/Emphasis-amino acid oxidase activity
机译:FSTL1 aggravates OVA-induced inflammatory responses by activating the NLRP3/IL-1 beta signaling pathway in mice and macrophages
机译:A role for peroxisome proliferator-activated receptor alpha (PPARalpha ) in the control of cardiac malonyl-CoA levels: reduced fatty acid oxidation rates and increased glucose oxidation rates in the hearts of mice lacking PPARalpha are associated wit
机译:Increasing levels of circulating Th17 cells and interleukin-17 in rheumatoid arthritis patients with an inadequate response to anti-TNF-alpha therapy