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.
"Clinical symptoms of food allergy patients range from a mild skin reaction to lethal shock (Boyce et al., 2010; Sicherer and Sampson, 2010). The anaphylactic response to ingested food antigens usually results from the activation of intestinal mast cells (MCs) through food-specific IgE antibodies (Finkelman, 2007; Galli and Tsai, 2012). However, it is perplexing as to why only some patients and murine strains that acquire high amounts of dietary allergen-specific IgE develop a severe immediate intestinal hypersensitivity response that can result in life-threatening anaphylaxis. "
[Show abstract][Hide abstract] ABSTRACT: Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin-9 (IL-9). However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9- and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy.
"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. "
"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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