UV-mediated regulation of antimicrobial peptides

该项目基于这样的假设，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，我们推测，AMP除了具有抗微生物活性外，还有助于抑制获得性免疫反应。利用变态反应性接触性超敏反应模型，我们证明了小鼠AMP？防御素-14(MBD-14)可诱导抗原特异性调节性T细胞(Treg)。与主要影响抗原呈递细胞的紫外线照射不同，MBD-14直接针对T细胞。因此，续期拨款将阐明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是否在其他免疫模型(变应性自身免疫性脑炎)中也发挥免疫抑制作用，以及人类AMP是否也可以诱导Treg。

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.