太阳可以暖和皮肤,可能也可以让人类免受疾病困扰,来自斯坦福大学的Hekla Sigmundsdottir、Junliang Pan和他们的同事称。此项研究成果发表在近日的《Nature Immunol.》杂志上,感兴趣的读者可以参看英文原文。
研究小组让树突细胞——一类免疫细胞——暴露在维生素D之下(维生素D是皮肤在阳光下可以自发合成的)。维生素可以刺激树突细胞,同时还可以刺激T细胞(另外一类免疫细胞),刺激它们将维生素D转化为化学上的活化状态。这种活化态的维生素D诱导T细胞在细胞表面表达一些特殊的“归巢分子”(homing molecule),并在这些分子的引导下,T细胞聚集到皮肤组织。
作者认为通过这种机制,阳光可以激发免疫系统通过T细胞来保护皮肤组织免受伤害,例如阻挡致病菌的入侵,修复太阳造成的损伤,等等。
一项新的研究结果表明:阳光能够通过将免疫细胞吸引到皮肤的表层从而达到抵抗皮肤疾病和抗癌的效果。
美国加州斯坦福大学的Eugene Butcher及其同事们发现了人类皮肤中一个有趣的免疫过程。皮肤中被称为树突状细胞的免疫细胞能够将维生素D3(在皮肤暴露于阳光时产生)转化为其活性形式。Butcher的研究小组发现:这种活跃的维生素D3会使得T细胞迁移到皮肤的最表层。T细胞是能够杀死损坏细胞和感染细胞的免疫细胞,它们也会控制其他的免疫细胞。
研究人员表示:该发现解释了一旦皮肤遭受了某种太阳激发 DNA 损伤,T细胞如何获知并到达皮肤表层的原因。
参与研究的Hekla Sigmundsdottir表示:只要不过量,阳光对人类健康有益。她指出牛皮癣有时可以通过使用维生素D3软膏治愈,据她推测可能就是通过将T细胞吸引到了皮肤表层而起到了作用。
(译自:newscientist)
部分英文原文:
DCs metabolize sunlight-induced vitamin D3 to 'program' T cell attraction to the epidermal chemokine CCL27
Hekla Sigmundsdottir1, 2, 4, Junliang Pan1, 2, 4, Gudrun F Debes1, 2, Carsten Alt1, 2, Aida Habtezion1, 2, Dulce Soler3 & Eugene C Butcher1, 2
1 Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
2 The Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA.
3 Millennium Pharmaceuticals, Cambridge, Massachusetts 02139, USA.
4 These authors contributed equally to this work.
Correspondence should be addressed to Eugene C Butcher ebutcher@stanford.edu
During adaptive immune responses, dendritic cells activate T cells and endow them with specific homing properties. Mechanisms that 'imprint' specific tropisms, however, are not well defined. We show here that 1,25(OH)2D3, the active form of vitamin D3, signaled T cells to express CC chemokine receptor 10, which enabled them to migrate to the skin-specific chemokine CCL27 secreted by keratinocytes of the epidermis. In contrast, 1,25(OH)2D3 suppressed the gut-homing receptors 47 and CCR9. Vitamin D3, the inactive prohormone naturally generated in the skin by exposure to the sun, was processed by dendritic cells and T cells to the active metabolite, providing a mechanism for the local regulation of T cell 'epidermotropism'. Our findings support a model in which dendritic cells process and 'interpret' locally produced metabolites to 'program' T cell homing and microenvironmental positioning.
更多原文链接:http://www.nature.com/ni/journal/vaop/ncurrent/abs/ni1433.html