太陽可以暖和皮膚，可能也可以讓人類免受疾病困擾,，來自斯坦福大學(xué)的Hekla Sigmundsdottir,、Junliang Pan和他們的同事稱。此項(xiàng)研究成果發(fā)表在近日的《Nature Immunol.》雜志上,，感興趣的讀者可以參看英文原文,。
研究小組讓樹突細(xì)胞——一類免疫細(xì)胞——暴露在維生素D之下(維生素D是皮膚在陽光下可以自發(fā)合成的)。維生素可以刺激樹突細(xì)胞,，同時(shí)還可以刺激T細(xì)胞（另外一類免疫細(xì)胞）,，刺激它們將維生素D轉(zhuǎn)化為化學(xué)上的活化狀態(tài),。這種活化態(tài)的維生素D誘導(dǎo)T細(xì)胞在細(xì)胞表面表達(dá)一些特殊的“歸巢分子”（homing molecule），并在這些分子的引導(dǎo)下,，T細(xì)胞聚集到皮膚組織,。
作者認(rèn)為通過這種機(jī)制，陽光可以激發(fā)免疫系統(tǒng)通過T細(xì)胞來保護(hù)皮膚組織免受傷害,，例如阻擋致病菌的入侵,，修復(fù)太陽造成的損傷，等等,。
一項(xiàng)新的研究結(jié)果表明：陽光能夠通過將免疫細(xì)胞吸引到皮膚的表層從而達(dá)到抵抗皮膚疾病和抗癌的效果,。
美國(guó)加州斯坦福大學(xué)的Eugene Butcher及其同事們發(fā)現(xiàn)了人類皮膚中一個(gè)有趣的免疫過程。皮膚中被稱為樹突狀細(xì)胞的免疫細(xì)胞能夠?qū)⒕S生素D3（在皮膚暴露于陽光時(shí)產(chǎn)生）轉(zhuǎn)化為其活性形式,。Butcher的研究小組發(fā)現(xiàn)：這種活躍的維生素D3會(huì)使得T細(xì)胞遷移到皮膚的最表層,。T細(xì)胞是能夠殺死損壞細(xì)胞和感染細(xì)胞的免疫細(xì)胞，它們也會(huì)控制其他的免疫細(xì)胞,。
研究人員表示：該發(fā)現(xiàn)解釋了一旦皮膚遭受了某種太陽激發(fā) DNA 損傷,，T細(xì)胞如何獲知并到達(dá)皮膚表層的原因。
參與研究的Hekla Sigmundsdottir表示：只要不過量,，陽光對(duì)人類健康有益,。她指出牛皮癬有時(shí)可以通過使用維生素D3軟膏治愈，據(jù)她推測(cè)可能就是通過將T細(xì)胞吸引到了皮膚表層而起到了作用,。
（譯自：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 [email protected]
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.
更多原文鏈接：http://www.nature.com/ni/journal/vaop/ncurrent/abs/ni1433.html
