Article

IgE and mast cells in allergic disease

Department of Pathology, Stanford University School of Medicine, California, USA.
Nature medicine (Impact Factor: 28.05). 05/2012; 18(5):693-704. DOI: 10.1038/nm.2755
Source: PubMed

ABSTRACT Immunoglobulin E (IgE) antibodies and mast cells have been so convincingly linked to the pathophysiology of anaphylaxis and other acute allergic reactions that it can be difficult to think of them in other contexts. However, a large body of evidence now suggests that both IgE and mast cells are also key drivers of the long-term pathophysiological changes and tissue remodeling associated with chronic allergic inflammation in asthma and other settings. Such potential roles include IgE-dependent regulation of mast-cell functions, actions of IgE that are largely independent of mast cells and roles of mast cells that do not directly involve IgE. In this review, we discuss findings supporting the conclusion that IgE and mast cells can have both interdependent and independent roles in the complex immune responses that manifest clinically as asthma and other allergic disorders.

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    • "Allergic symptoms such as edema, warmth, and erythema are resulted from vasodilation and an increase of vascular permeability caused by histamine . (Galli and Tsai, 2012) In the histamine and β-hexosaminidase assay using cell line (RBL-2H3) and primary cells (RPMCs), TMB strongly inhibited mast cell degranulation. OVA-induced ASA and IgE-mediated PCA models are positively associated with histamine release from mast cells. "
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    • "In aggregate, the notion remains that S1P may serve as a pro-inflammatory signal by promoting T cell effector differentiation and by suppressing T-regs, a T cell subset that also modulates antigen-induced responses in mast cells (Gri et al., 2008). This may be particularly relevant in cases of recurrent allergic reactions such as those seen with allergic asthma (Galli and Tsai, 2012), where repeated increases in S1P (and other mediators) produced by mast cells can thus contribute to chronic inflammation. In addition, the repeated challenges inherent to chronic allergic diseases cause tissue remodeling characterized by epithelial cell injury and structural changes in vascular, smooth muscle and connective tissues, many of which have been shown to be affected by S1P (reviewed in (Ryan and Spiegel, 2008)). "
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    • "Recently developed anti-IgE preventive therapies that neutralize circulating IgE or deplete IgE-producing cells have demonstrated some efficacy. However, clinical indications for these treatments have been limited to allergic asthma, chronic idiopathic urticarial , and rhinitis (Galli and Tsai, 2012; Gauvreau et al., 2014; Saini et al., 2015). Thus, the IgE oligomannose may be a potential therapeutic target for both cell-bound and circulating IgE. "
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