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体内暴露于紫外线照射的尿刊酸的表皮细胞诱导对单纯疱疹病毒迟发型超敏反应的抑制。

Induction of suppression of delayed type hypersensitivity to herpes simplex virus by epidermal cells exposed to UV-irradiated urocanic acid in vivo.

作者信息

Ross J A, Howie S E, Norval M, Maingay J P

机构信息

Department of Clinical and Laboratory Haematology, Western General Hospital, Edinburgh, Scotland.

出版信息

Viral Immunol. 1987;1(3):191-8. doi: 10.1089/vim.1987.1.191.

Abstract

Urocanic acid (UCA), the putative photoreceptor for ultraviolet radiation (UV)-induced suppression, undergoes a UV-dependent trans to cis isomerisation. Epidermal cells from mice painted with UCA, containing a known proportion of the cis-isomer, generate suppression of the delayed type hypersensitivity response to herpes simplex virus type 1 (HSV-1) when transferred to naive syngeneic recipients at the same time and site as infection with HSV-1. One T suppressor cell subset, of phenotype (Thy1+, L3T4+, Ly2-), is induced by the cis-UCA modified epidermal cell transfer. Flow cytometric analysis of the epidermal cells from skin treated with UV or cis-UCA indicates an overall reduction from normal in the number of cells expressing MHC Class II antigens, but no alteration in the number expressing I-J antigens.

摘要

尿刊酸(UCA)是紫外线(UV)诱导免疫抑制的假定光感受器,会发生紫外线依赖的反式到顺式异构化。用含有已知比例顺式异构体的UCA涂抹的小鼠表皮细胞,当在与单纯疱疹病毒1型(HSV-1)感染相同的时间和部位转移到同基因的未致敏受体时,会对HSV-1产生迟发型超敏反应的抑制。一种表型为(Thy1 +、L3T4 +、Ly2 -)的T抑制细胞亚群由顺式-UCA修饰的表皮细胞转移诱导产生。对经紫外线或顺式-UCA处理的皮肤的表皮细胞进行流式细胞术分析表明,表达MHC II类抗原的细胞数量总体上比正常减少,但表达I-J抗原的细胞数量没有改变。

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