For the maintenance of homeostasis termination of immune reactions is as equally important as their induction. In this scenario regulatory T cells (Treg) play an important role. Accordingly a variety of inflammatory diseases are caused by an impairment of Treg. Hence, it is important to identify triggers by which Treg can be induced and activated, respectively. For quite a long time it is known that ultraviolet radiation can induce Treg which inhibit cutaneous immune reactions including contact hypersensitivity. Since these Treg inhibit in an antigen-specific fashion they may harbor therapeutic potential. However similar Treg can be induced also by other triggers which include vitamin D and antimicrobial peptides. Recently it was discovered that the gut microbiome controls the development of Treg in the intestine. The same may apply for the skin. Short chain fatty acids, microbiota-derived bacterial fermentation products, appear to induce and to activate Treg in the skin. Topical application of short chain fatty acids was shown to inhibit contact hypersensitivity and to reduce inflammation in the murine imiquimod-induced psoriasis-like skin inflammation model. Together, these data indicate that induction and activation of Treg may be a potential therapeutic strategy to treat inflammatory diseases in the future.

中文翻译：

---

皮肤调节性 T 细胞的控制器：紫外线辐射和皮肤微生物组

为了维持体内平衡，免疫反应的终止与它们的诱导同样重要。在这种情况下，调节性 T 细胞 (Treg) 发挥着重要作用。因此，多种炎性疾病是由Treg的损伤引起的。因此，重要的是确定可以分别诱导和激活 Treg 的触发器。很长一段时间以来，人们都知道紫外线辐射可以诱导 Treg，从而抑制皮肤免疫反应，包括接触过敏。由于这些 Treg 以抗原特异性方式抑制，它们可能具有治疗潜力。然而，类似的 Treg 也可以由包括维生素 D 和抗微生物肽在内的其他触发因素诱导。最近发现肠道微生物组控制肠道中 Treg 的发育。这同样适用于皮肤。短链脂肪酸，微生物群衍生的细菌发酵产物，似乎可以诱导和激活皮肤中的 Treg。在小鼠咪喹莫特诱导的银屑病样皮肤炎症模型中，局部应用短链脂肪酸可抑制接触超敏反应并减少炎症。总之，这些数据表明 Treg 的诱导和激活可能是未来治疗炎症性疾病的潜在治疗策略。