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. 2000 Oct 16;192(8):1093–1104. doi: 10.1084/jem.192.8.1093

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© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Model of Th2 cytokine–mediated homeostasis in mast cell inflammatory responses. Initial production of IL-4 and IL-10 elicits IgE synthesis and mast cell proliferation. IgE–antigen interactions activate mast cells, causing production of inflammatory mediators, with the resulting sequelae noted in allergic disease. This process may be reversed after 3 d, when IL-4 and IL-10 inhibit FcεRI and Kit function, and ultimately induce apoptosis of both mature mast cells and mast cell precursors. The result is a balance of pro- and antiinflammatory reactions, yielding time-limited mast cell hyperplasia and inflammatory reactions coordinated by the Th2 cytokines IL-4 and IL-10.