Oxaliplatin-Associated Amaurosis Fugax

Oxaliplatin-associated amaurosis fugax has not been reported, and its clinical course and treatment remain largely unclear. A 70-year-old man with advanced gastric cancer was treated with the SOX regimen. After cycle 1 of oxaliplatin infusion, the patient realized that his right eye had visual field impairment, which he described as darkening of the right half of his visual field and loss of vision lasting about 1 min and occurring about 7 times a day. The daily frequency of this occurrence gradually decreased, and his visual field impairment improved in 1 week. However, as the same symptoms recurred from cycle 2 to cycle 5 of treatment, oxaliplatin was discontinued from cycle 6 and switched to S-1 monotherapy. Subsequently, the patient’s amaurosis fugax improved. To our knowledge, this is the first report describing clinical course and treatment of oxaliplatin-associated amaurosis fugax

多発性硬化症において、血中のエクソソームが、let-7iを介して制御性T細胞の分化を抑制する

京都大学0048新制・課程博士博士(医学)甲第21020号医博第4366号新制||医||1028(附属図書館)京都大学大学院医学研究科医学専攻(主査)教授 椛島 健治, 教授 三森 経世, 教授 小柳 義夫学位規則第4条第1項該当Doctor of Medical ScienceKyoto UniversityDFA

The Role for Exosomal microRNAs in Disruption of Regulatory T Cell Homeostasis in Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, in which myelin and oligodendrocytes are the main targets recognized by inflammatory CD4 + T cells reactive to myelin peptides. Regulatory CD4 + T (Treg) cells normally keep homeostasis of the immune system by inhibiting detrimental effects of inflammatory T cells. However, Treg cells are reduced in patients with MS for unknown reason. This commentary highlights a novel function of circulating exosomes to inhibit the differentiation of Treg cells in MS. Our recent work has demonstrated that the circulating exosomes, a member of extracellular vesicles, of patients with MS exert this effect by transferring let-7i to naive CD4 + T cells. The transferred let-7i subsequently causes a decreased expression of insulin like growth factor 1 receptor (IGF1R) and transforming growth factor β receptor 1 (TGFBR1), leading to the inhibition of Treg cell differentiation. Thus, extrinsic microRNAs transferred by exosomes might have an active role in triggering autoimmune diseases. We hypothesize that extracellular vesicles including exosomes can be a communication tool between the gut microbiota and the host immune system. Further research in this area will expand the knowledge about the precise mechanism of autoimmune diseases and can lead to a new therapeutic approach