Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 163-169 |
| Number of pages | 7 |
| Journal | Blood Reviews |
| Volume | 24 |
| Issue number | 4-5 |
| DOIs | |
| Publication status | Published - Jul 2010 |
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