Maternal signals for progeny prevention against allergy and asthma

被引:5
|
作者
Marsh, Leigh Matthew [2 ]
Pfefferle, Petra Ina [2 ]
Pinkenburg, Olaf [2 ]
Renz, Harald [1 ]
机构
[1] Univ Marburg, Fac Med, Inst Lab Med & Pathobiochem, D-35043 Marburg, Germany
[2] Univ Marburg, Dept Clin Chem & Mol Diagnost, D-35043 Marburg, Germany
关键词
Allergy; Asthma; Toll-like receptors; Innate immune system; Allergy protection; Prenatal; Animal model; NEONATAL IMMUNE-RESPONSES; T-CELL DIFFERENTIATION; IFN-GAMMA PROMOTER; DNA METHYLATION; GENE-EXPRESSION; CORD BLOOD; HIGH-RISK; HISTONE MODIFICATIONS; AIRWAY INFLAMMATION; CYTOKINE PRODUCTION;
D O I
10.1007/s00018-011-0644-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Allergy and asthma are chronic inflammatory diseases which result from complex gene-environment interactions. Recent evidence indicates the importance of prenatal and postnatal developmental processes in terms of maturation of balanced immune responses. According to the current view, gene-environment interactions during a restricted time frame are responsible for programming of the immune system in favor of allergic immune mechanisms later in life. The interaction between genes and environment is complex and only partially understood; however, heritable epigenetic modifications including chemical additions in and alternative packaging of the DNA have been shown to play a crucial role in this context. Novel data indicate that epigenetic mechanisms contribute to the development of T-helper cell function. Environmental factors, including diesel exhaust particles (DEP), vitamins and tobacco smoke, operate through such mechanisms. Furthermore, the role of environmental microbes provides another and maybe even more important group of exogenous exposures which operates in this critical time frame.
引用
收藏
页码:1851 / 1862
页数:12
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