Article

IgE and mast cells in allergic disease

Department of Pathology, Stanford University School of Medicine, California, USA.
Nature medicine (Impact Factor: 27.36). 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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    • "We recently demonstrated that the function of cell adhesion is conserved in mammalian Notch family members[14,15]. Our first objective was to determine the role of Notch signaling in mammalian mast cells, a hematopoietic cell lineage that is best known for its roles in the mediation of allergic inflammation[69]. Notch receptors are widely expressed among mammalian immune cells, including mast cells, and control their differentiation and functions707172. "
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    ABSTRACT: Notch family members are generally recognized as signaling molecules that control various cellular responses in metazoan organisms. Early fly studies and our mammalian studies demonstrated that Notch family members are also cell adhesion molecules; however, information on the physiological roles of this function and its origin is limited. In this review, we discuss the potential present and ancestral roles of Notch-mediated cell adhesion in order to explore its origin and the initial roles of Notch family members dating back to metazoan evolution. We hypothesize that Notch family members may have initially emerged as cell adhesion molecules in order to mediate multicellularity in the last common ancestor of metazoan organisms.
    Full-text · Article · Jan 2016 · Biology
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    • "Mast cells (MC) convey immunomodulatory functions through their unique ability to release, after activation, many mediators including cytokines, chemokines, and enzymes, some of which are prestored in cytoplasmic granules at homeostasis [1]. MC are bona fide sentinels present in most vascularized tissues prior to trauma, equipped with a vast selection of surface receptors, therefore sensing and quickly responding to local alterations [2]. "
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    ABSTRACT: Mast cells (MC) are present in most vascularized tissues around the vasculature likely exerting immunomodulatory functions. Endowed with diverse mediators, resident MC represent first-line fine-tuners of local microenvironment. Sphingosine-1-phosphate (S1P) functions as a pluripotent signaling sphingolipid metabolite in health and disease. S1P formation occurs at low levels in resting MC and is upregulated upon activation. Its export can result in type 2 S1P receptor- (S1PR2-) mediated stimulation of MC, further fueling inflammation. However, the role of S1PR2 ligation in proangiogenic vascular endothelial growth factor- (VEGF-) A and matrix metalloproteinase- (MMP-) 2 release from MC is unknown. Using a preclinical MC-dependent model of acute allergic responses and in vitro stimulated primary mouse bone marrow-derived MC (BMMC) or human primary skin MC, we report that S1P signaling resulted in substantial amount of VEGF-A release. Similar experiments using S1pr2 -deficient mice or BMMC or selective S1P receptor agonists or antagonists demonstrated that S1P/S1PR2 ligation on MC is important for VEGF-A secretion. Further, we show that S1P stimulation triggered transcriptional upregulation of VEGF-A and MMP-2 mRNA in human but not in mouse MC. S1P exposure also triggered MMP-2 secretion from human MC. These studies identify a novel proangiogenic axis encompassing MC/S1P/S1PR2 likely relevant to inflammation.
    Full-text · Article · Jan 2016 · Mediators of Inflammation
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    • "Mast cells are the most important effector cells in inflammatory and allergic diseases[1]. Thus, researchers concerning mast cells should focus on their detrimental pathologic effects. "
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    ABSTRACT: To investigate the antihistamine-releasing effect of a peptide isolated from wasp venom of Vespa orientalis.
    Full-text · Article · Jan 2016 · Asian Pacific Journal of Tropical Biomedicine
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