東京大学 · 医学
Shinsuke Yasuda教授の研究室は、自己免疫疾患、特にSystemic Lupus Erythematosus（SLE）や抗磷脂質症候群（APS）の分子メカニズムを解明することを主眼としています。RasGRP1の機能異常やβ2-グリコプロテインI（β2-GPI）の変異・修飾が自己抗体の産生や自己免疫反応に与える影響を遺伝子・タンパク質レベルで解析しています。また、GLP-1レセプター作動薬が筋炎性疾患の治療に有効である可能性についても、細胞死の制御を軸に研究を展開しています。
Figures are computed from collected data and may differ slightly.
Dysregulation of Ras guanyl nucleotide-releasing protein 1 (RasGRP1) in mice results in a systemic lupus erythematosus (SLE)-like disorder. We therefore looked for defective isoforms and/or diminished levels of human RasGRP1 in a cohort of SLE patients. PBMCs were collected from twenty healthy individuals and thirty-two patients with SLE. mRNA was isolated and five RasGRP1 cDNAs from each subject were sequenced. T cell lysates from healthy controls and SLE patients also were evaluated for their
BEta(2)-glycoprotein I (beta(2)-GPI) is proteolytically cleaved by plasmin in domain V (nicked beta(2)-GPI), being unable to bind to phospholipids. This cleavage may occur in vivo and elevated plasma levels of nicked beta(2)-GPI were detected in patients with massive plasmin generation and fibrinolysis turnover. In this study, we report higher prevalence of elevated ratio of nicked beta(2)-GPI against total beta(2)-GPI in patients with ischemic stroke (63%) and healthy subjects with lacunar infa
The Val(247) beta(2)GPI allele was associated with both a high frequency of anti-beta(2)GPI antibodies and stronger reactivity with anti-beta(2)GPI antibodies compared with the Leu(247) beta(2)GPI allele, suggesting that the Val(247) beta(2)GPI allele may be one of the genetic risk factors for development of APS.
GLP-1R agonist could be a novel therapy for PM that recovers muscle weakness and suppresses muscle inflammation through inhi biting muscle fibre necroptosis.
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