Understanding the genetic regulation of IgE production

被引：22

作者：

Altin, John ^{[1
]}

Shen, Chong ^{[2
]}

Liston, Adrian ^{[2
,3
]}

机构：

[1] Australian Natl Univ, John Curtin Sch Med Res, Canberra, ACT 0200, Australia

[2] VIB, B-9052 Ghent, Belgium

[3] Univ Leuven, B-3000 Louvain, Belgium

来源：

BLOOD REVIEWS | 2010年 / 24卷 / 4-5期

关键词：

IgE; Genetic regulation; Genomics; Atopy; Immune tolerance; WISKOTT-ALDRICH-SYNDROME; INTERFERON-GAMMA-RECEPTOR; 22Q11.2 DELETION SYNDROME; IMMUNOGLOBULIN-E LEVELS; T-CELLS; PROMOTER POLYMORPHISM; ASSOCIATION ANALYSIS; QUANTITATIVE TRAITS; ATOPIC-DERMATITIS; ALLERGIC DISEASE;

D O I：

10.1016/j.blre.2010.06.002

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

Immunoglobulin E (IgE) is a key mediator of anti-parasitic and anti-tumour immunity. However it is also a critical component of atopic and autoimmune diseases, and elevated serum IgE levels are a common indicator of immune dysregulation. In this review we survey the literature on genetic associations of elevated IgE in humans and mice. We find that defects in a limited number of pathways explain the majority of gene associations with IgE. Commonly, elevated IgE is associated with defects in Th bias and B cell class switching, severe T cell tolerance defects and defects in immunity at the host-environment interface. These genetic data demonstrate the mechanisms of control over IgE production and the manner in which they can be circumvented. (C) 2010 Elsevier Ltd. All rights reserved.

引用

收藏

页码：163 / 169

页数：7

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