Science2014-06-13 4:34 PM

即使缺乏其所需的维生素,免疫细胞仍然可以保护宿主 Adaptation of Innate Lymphoid Cells to a Micronutrient Deficiency Promotes Type 2 Barrier Immunity

论文摘要 

营养不良会损害免疫系统,降低其强度与力量,但如今一项新的研究显示,世界上最常见的营养不良问题之一--维生素A的缺乏--可提升某种关键性免疫细胞的水平。在世界上那些常见的营养不良地区,寄生性蠕虫感染也可能是普遍的。这就需要所谓的在粘膜表面的屏障免疫--这是一种部分由先天淋巴样细胞(ILCs)介导的免疫策略。ILCs似乎会对维生素A提供的信号--具体地说是该维生素的一个叫做视黄酸(RA)的代谢物--做出反应。为了更好地理解视黄酸是如何影响某些ILCs的生长的,S.P. Spencer及其同事在维生素A缺乏的小鼠(在这些小鼠中,RA信号传导是阙如的)中研究了ILCs亚群的行为。他们发现,在这些小鼠中,ILC的某些亚群(即那些对细菌免疫重要的亚群)大大地减少了,而另外某些亚群,尤其是ILC2s,则出现数目的增长(后来发现,ILC2s因缺乏RA受体而可在没有维生素A存在的情况下增生。它们对保护机体免受寄生性蠕虫感染起着重要的作用)。Spencer及其同事的结果显示机体会如何切换到一种不同的免疫类型,即使当机体缺乏重要的营养资源时也能让宿主活着。维生素A缺乏会使免疫系统倾斜,使得它做好准备以保护机体免受寄生性蠕虫的感染,而后者是维生素A缺乏症流行地区的一个重大问题。

Abstract 

How the immune system adapts to malnutrition to sustain immunity at barrier surfaces, such as the intestine, remains unclear. Vitamin A deficiency is one of the most common micronutrient deficiencies and is associated with profound defects in adaptive immunity. Here, we found that type 3 innate lymphoid cells (ILC3s) are severely diminished in vitamin A–deficient settings, which results in compromised immunity to acute bacterial infection. However, vitamin A deprivation paradoxically resulted in dramatic expansion of interleukin-13 (IL-13)–producing ILC2s and resistance to nematode infection in mice, which revealed that ILCs are primary sensors of dietary stress. Further, these data indicate that, during malnutrition, a switch to innate type 2 immunity may represent a powerful adaptation of the immune system to promote host survival in the face of ongoing barrier challenges.

Editor's Summary

An Immune Response to Malnutrition

Mucosal surfaces, such as those lining the intestine, are in constant contact with potentially pathogenic microbes, including bacteria and parasitic worms. This necessitates so-called barrier immunity, which is mediated in part by innate lymphoid cells, subsets of which combat specific types of infection. Although malnutrition has been associated with immunosuppression, Spencer et al. (p. 432) now show that vitamin A deficiency selectively activates one branch of barrier immunity. Vitamin A deficiency in mice enhanced immunity to chronic worm infections by increasing the levels of one subset of innate lymphoid cells lacking the corresponding retinoic acid receptor. In contrast, another innate lymphoid cell subset that carries the vitamin A receptor and is important for bacterial immunity was depleted. Thus, the immune system can adapt its response to dietary stress, thereby promoting host survival.

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