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The Multitasking Mast Cell: Positive and Negative Roles in the Progression of Autoimmunity

Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611

Among the potential outcomes of an aberrantly functioning immune system are allergic disease and autoimmunity. Although it has been assumed that the underlying mechanisms mediating these conditions are completely different, recent evidence shows that mast cells provide a common link. Mast cells reside in most tissues, are particularly prevalent at sites of Ag entry, and act as sentinel cells of the immune system. They express many inflammatory mediators that affect both innate and adaptive cellular function. They contribute to pathologic allergic inflammation but also serve an important protective role in bacterial and parasite infections. Given the proinflammatory nature of autoimmune responses, it is not surprising that studies using murine models of autoimmunity clearly implicate mast cells in the initiation and/or progression of autoimmune disease. In this review, we discuss the defined and hypothesized mechanisms of mast cell influence on autoimmune diseases, including their surprising and newly discovered role as anti-inflammatory cells.

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¹ Address correspondence and reprint requests to Dr. Melissa A. Brown, Department of Microbiology and Immunology, 303 East Superior Street, Tarry Building 6-701, Northwestern University Feinberg School of Medicine, Chicago, IL 60611. E-mail address: m-brown12{at}northwestern.edu

² Abbreviations used in this paper: DC, dendritic cell; CRH, corticotropin-releasing hormone; EAE, experimental allergic/autoimmune encephalomyelitis; MS, multiple sclerosis; NGF, nerve growth factor; PAR-2, protease activated receptor 2; RA, rheumatoid arthritis; Tr1, T regulatory type 1 cell; Treg, regulatory T cell.

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