UV-mediated regulation of antimicrobial peptides

紫外线介导的抗菌肽调节

• 批准号: 153090838
• 负责人: Professor Dr. Thomas Schwarz
• 金额: --
• 依托单位: Klinik für Dermatologie, Venerologie und Allergologie
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2010
• 资助国家: 德国
• 起止时间: 2009-12-31 至 2015-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/153090838?language=en
• 关键词: UV; mediated; regulation; antimicrobial; peptides

This project is based on the hypothesis that the well known suppression of T-cell-mediated immune reactions by ultraviolet radiation (UVR) is as beneficial as the induction of antimicrobial peptides (AMP), since this could inhibit allergic and autoimmune reactions in the skin. Hence, we postulated that AMP in addition to their antimicrobial activity contribute also to the suppression of the adaptive immune response. Utilizing the model of allergic contact hypersensitivity we showed that the murine AMP ß-defensin-14 (mBD-14) induces antigen-specific regulatory T cells (Treg). In contrast to UVR which primarily affects antigen-presenting cells, mBD-14 targets directly T cells. Thus, the renewal grant shall clarify by which mechanisms mBD-14 induces Treg, to what extent mBD-14-induced Treg differ from UVR-induced Treg, whether mBD-14 exerts its immunosuppressive features also in other immunologic models (allergic autoimmune encephalitis) and whether human AMP can induce Treg as well.

该项目基于一个假设，即众所周知的紫外线辐射（UVR）对t细胞介导的免疫反应的抑制与抗菌肽（AMP）的诱导一样有益，因为这可以抑制皮肤中的过敏和自身免疫反应。因此，我们假设AMP除了具有抗菌活性外，还有助于抑制适应性免疫反应。利用变态反应性接触超敏反应模型，我们发现小鼠AMP ß-防御素-14 （mBD-14）诱导抗原特异性调节性T细胞（Treg）。与UVR主要影响抗原呈递细胞不同，mBD-14直接靶向T细胞。因此，续期资助应明确mBD-14诱导Treg的机制，mBD-14诱导的Treg与uvr诱导的Treg有何不同，mBD-14是否也在其他免疫模型（过敏性自身免疫性脑炎）中发挥其免疫抑制功能，以及人AMP是否也可以诱导Treg。