Linking iron-deficiency with allergy: role of molecular allergens and the microbiome,Metallomics

当前位置： X-MOL 学术 › Metallomics › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Linking iron-deficiency with allergy: role of molecular allergens and the microbiome
Metallomics ( IF 2.9 ) Pub Date : 2017-11-09 00:00:00 , DOI: 10.1039/c7mt00241f
Franziska Roth-Walter _{1,

2,

3,

4,

5} , Luis F. Pacios _{6,

7,

8,

9,

10} , Rodolfo Bianchini _{1,

2,

3,

4,

5} , Erika Jensen-Jarolim _{1,

2,

3,

4,

5}

Affiliation

Atopic individuals tend to develop a Th2 dominant immune response, resulting in hyperresponsiveness to harmless antigens, termed allergens. In the last decade, epidemiological studies have emerged that connected allergy with a deficient iron-status. Immune activation under iron-deficient conditions results in the expansion of Th2-, but not Th1 cells, can induce class-switching in B-cells and hampers the proper activation of M2, but not M1 macrophages. Moreover, many allergens, in particular with the lipocalin and lipocalin-like folds, seem to be capable of binding iron indirectly via siderophores harboring catechol moieties. The resulting locally restricted iron-deficiency may then lead during immune activation to the generation of Th2-cells and thus prepare for allergic sensitization. Moreover, iron-chelators seem to also influence clinical reactivity: mast cells accumulate iron before degranulation and seem to respond differently depending on the type of the encountered siderophore. Whereas deferoxamine triggers degranulation of connective tissue-type mast cells, catechol-based siderophores reduce activation and degranulation and improve clinical symptoms. Considering the complex interplay of iron, siderophores and immune molecules, it remains to be determined whether iron-deficiencies are the cause or the result of allergy.

中文翻译：

将铁缺乏症与过敏联系起来：分子过敏原和微生物组的作用

特应性个体倾向于产生Th2显性免疫反应，导致对称为过敏原的无害抗原过敏。在过去的十年中，流行病学研究已经出现，这些研究将过敏与铁缺乏状态联系在一起。缺铁条件下的免疫激活导致Th2细胞（而非Th1细胞）扩增，可诱导B细胞的类别转换，并阻碍M2而不是M1巨噬细胞的正确激活。此外，许多变应原，特别是具有脂钙蛋白和脂钙蛋白样褶皱的变应原，似乎能够通过以下方式间接结合铁邻苯二酚含有邻苯二酚部分。然后，在免疫激活过程中，导致的局部限制性铁缺乏症可能导致Th2-细胞的生成，从而为过敏性致敏做好准备。此外，铁螯合剂似乎也影响临床反应性：肥大细胞在脱粒之前会积聚铁，并且根据遇到的铁载体的类型似乎会有不同的反应。去铁胺可引起结缔组织型肥大细胞脱颗粒，而基于儿茶酚的铁载体可减少活化和脱颗粒并改善临床症状。考虑到铁，铁载体和免疫分子之间的复杂相互作用，铁缺乏是过敏的原因还是结果仍有待确定。

更新日期：2017-11-09

点击分享查看原文

点击收藏

公开下载

阅读更多本刊最新论文本刊介绍/投稿指南11