会员体验
专利管家(专利管理)
工作空间(专利管理)
风险监控(情报监控)
数据分析(专利分析)
侵权分析(诉讼无效)
联系我们
交流群
官方交流:
QQ群: 891211   
微信请扫码    >>>
现在联系顾问~
热词
    • 6. 发明授权
    • Method for treating UV-induced suppression of contact hypersensitivity
by administration of T4 endonuclease
    • 通过施用T4内切核酸酶治疗UV诱导的接触性超敏反应抑制的方法
    • US5302389A
    • 1994-04-12
    • US931218
    • 1992-08-17
    • Margaret L. KripkeDaniel B. Yarosh
    • Margaret L. KripkeDaniel B. Yarosh
    • A61K8/14A61K8/66A61K9/127A61K38/46A61Q17/04A61Q19/00A61K37/22A61K37/54
    • A61K8/66A61K38/465A61K8/14A61K9/1272A61Q17/04A61Q19/00C12Y301/21002
    • Exposing the skin to UV radiation interferes with the induction of the T-cell mediated immune response, including both delayed (DHS) and contact (CHS) hyper-sensitivity immune responses initiated at non-irradiated sites. The present inventors have discovered that DNA is at least one of the targets for UV-induced hypersensitivity, and demonstrate that the application of DNA repair enzymes can reverse the damaging effects of UV irradiation on both the DHS and CHS response. The usefulness of the invention in this regard was tested using a model immunosuppression system in mice. In these studies, mice were first exposed to UV radiation and then liposomes were used to deliver a dimer-specific excision repair enzyme to their epidermis in situ. The application of liposomal T4 endonuclease V encapsulated to the UV-irradiated skin both decreased the number of cyclobutane pyrimidine dimers in the epidermis and prevented suppression of both delayed and contact hypersensitivity responses. Moreover, the formation of suppressor lymphoid cells was inhibited. These studies illustrate that the delivery of lesion-specific DNA repair enzymes to living skin after UV irradiation is an effective tool for restoring immune function and suggest that this approach may be broadly applicable to preventing other alterations caused by DNA damage, including preventing or reversing viral activation (e.g., herpes virus activation), oncogene expression, or autoimmune episodes.
    • 将皮肤暴露于紫外线辐射干扰T细胞介导的免疫应答的诱导,包括在非照射部位发起的延迟(DHS)和接触(CHS)超敏感性免疫应答。 本发明人已经发现,DNA是UV诱导的超敏反应的至少一个目标,并且证明DNA修复酶的应用可以逆转UV照射对DHS和CHS响应的破坏作用。 使用小鼠中的模型免疫抑制系统测试本发明在这方面的有用性。 在这些研究中,首先将小鼠暴露于紫外线辐射,然后使用脂质体将原位二聚体特异性切除修复酶递送至其表皮。 脂质体T4内切核酸酶V包封在紫外线照射皮肤上的应用减少了表皮中环丁烷嘧啶二聚体的数量,并阻止了延迟和接触超敏反应的抑制。 此外,抑制性淋巴样细胞的形成被抑制。 这些研究表明,紫外线照射后病毒特异性DNA修复酶对活体皮肤的传递是恢复免疫功能的有效工具,并表明该方法可广泛适用于预防DNA损伤引起的其他改变,包括预防或逆转病毒 激活(例如,疱疹病毒激活),癌基因表达或自身免疫发作。