• Theoharis C Theoharides, Konstantinos-Dionysios Alysandratos, Asimenia Angelidou, Danae-Anastasia Delivanis, Nikolaos Sismanopoulos, Bodi Zhang, Shahrzad Asadi, Magdalini Vasiadi, Zuyi Weng, Alexandra Miniati, and Dimitrios Kalogeromitros.
• Laboratory of Molecular Immunopharmacology and Drug Discovery, Department of Molecular Physiology and Pharmacology, Tufts University School of Medicine, Boston, MA 02111, USA. theoharis.theoharides@tufts.edu
• Biochim. Biophys. Acta. 2012 Jan 1; 1822 (1): 21-33.

AbstractMast cells are well known for their role in allergic and anaphylactic reactions, as well as their involvement in acquired and innate immunity. Increasing evidence now implicates mast cells in inflammatory diseases where they are activated by non-allergic triggers, such as neuropeptides and cytokines, often exerting synergistic effects as in the case of IL-33 and neurotensin. Mast cells can also release pro-inflammatory mediators selectively without degranulation. In particular, IL-1 induces selective release of IL-6, while corticotropin-releasing hormone secreted under stress induces the release of vascular endothelial growth factor. Many inflammatory diseases involve mast cells in cross-talk with T cells, such as atopic dermatitis, psoriasis and multiple sclerosis, which all worsen by stress. How mast cell differential responses are regulated is still unresolved. Preliminary evidence suggests that mitochondrial function and dynamics control mast cell degranulation, but not selective release. Recent findings also indicate that mast cells have immunomodulatory properties. Understanding selective release of mediators could explain how mast cells participate in numerous diverse biologic processes, and how they exert both immunostimulatory and immunosuppressive actions. Unraveling selective mast cell secretion could also help develop unique mast cell inhibitors with novel therapeutic applications. This article is part of a Special Issue entitled: Mast cells in inflammation.Copyright © 2010 Elsevier B.V. All rights reserved.

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