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ISSN 打印: 1040-8401
ISSN 在线: 2162-6472

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DOI: 10.1615/CritRevImmunol.v27.i1.20
pages 15-32

Mast Cell Homeostasis: A Fundamental Aspect of Allergic Disease

John J. Ryan
Department of Biology, Virginia Commonwealth University, Richmond, VA
Mohit Kashyap
Department of Biology, Virginia Commonwealth University, Richmond, VA
Daniel Bailey
Department of Biology, Virginia Commonwealth University, Richmond, VA
Sarah Kennedy
Department of Biology, Virginia Commonwealth University, Richmond, VA
Kelly Speiran
Department of Biology, Virginia Commonwealth University, Richmond, VA
Jennifer Brenzovich
Department of Biology, Virginia Commonwealth University, Richmond, VA
Brian Barnstein
Department of Biology, Virginia Commonwealth University, Richmond, VA
Carole Oskeritzian
Department of Biochemistry, Virginia Commonwealth University, Richmond, VA
Gregorio Gomez
Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA

ABSTRACT

Mast cells are well known for their role in allergic disease and have recently been implicated in inflammatory disorders, including autoimmune arthritis, multiple sclerosis, and atherosclerosis. Although aberrant mast cell activation is the focus of many studies, much less is known about normal mast cell homeostasis. Because loss of the normal constraints on mast cell activation, proliferation, and survival may be central to disease etiology, understanding these issues warrants attention. This review summarizes the knowledge of mast cell homeostasis controlled by IgE and the regulatory cytokines IL-4, IL-10, and TGF-β1. Because each of these proteins plays an important role in immune responses tied to mast cell-associated disease, this group represents a potential set of factors altered in atopic or autoimmune patients. It is interesting to note, for example, that polymorphisms within each of these factors or their receptors are linked to allergic disease. By first understanding how cytokines and IgE regulate mast cell function and survival, we may then predict how these factors may function in disease onset and progression.


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