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IgE and mast cells in host defense against parasites and venoms

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Abstract

IgE-dependent mast cell activation is a major effector mechanism underlying the pathology associated with allergic disorders. The most dramatic of these IgE-associated disorders is the fatal anaphylaxis which can occur in some people who have developed IgE antibodies to otherwise innocuous antigens, such as those contained in certain foods and medicines. Why would such a highly “maladaptive” immune response develop in evolution and be retained to the present day? Host defense against parasites has long been considered the only beneficial function that might be conferred by IgE and mast cells. However, recent studies have provided evidence that, in addition to participating in host resistance to certain parasites, mast cells and IgE are critical components of innate (mast cells) and adaptive (mast cells and IgE) immune responses that can enhance host defense against the toxicity of certain arthropod and animal venoms, including enhancing the survival of mice injected with such venoms. Yet, in some people, developing IgE antibodies to insect or snake venoms puts them at risk for having a potentially fatal anaphylactic reaction upon subsequent exposure to such venoms. Delineating the mechanisms underlying beneficial versus detrimental innate and adaptive immune responses associated with mast cell activation and IgE is likely to enhance our ability to identify potential therapeutic targets in such settings, not only for reducing the pathology associated with allergic disorders but perhaps also for enhancing immune protection against pathogens and animal venoms.

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Acknowledgments

We thank the past and current members of the Galli lab and the many collaborators who have made important contributions to the work reviewed herein. The work reviewed herein was supported by grants to S.J.G. from the National Institutes of Health (e.g., R37 AI23990, R01 CA072074, R01 AR067145, and U19 AI104209) and the National Science Foundation, and from several other funding sources, including the Department of Pathology at Stanford University. P.S. was supported by a Max Kade Fellowship of the Max Kade Foundation and the Austrian Academy of Sciences, a Schroedinger Fellowship of the Austrian Science Fund (FWF): J3399-B21, and a Marie Curie Fellowship of the European Commission (H2020-MSCA-IF-2014), 655153. T.M. was supported by a Marie Curie International Outgoing Fellowship for Career Development: European Union’s Seventh Framework Programme (FP7-PEOPLE-2011-IOF), 299954, and a “Charge de recherches” fellowship of the Belgian National Fund for Scientific Research (F.R.S-FNRS).

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Correspondence to Stephen J. Galli.

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Kaori Mukai and Mindy Tsai are co-first authors.

This article is a contribution to the special issue on Basophils and Mast Cells in Immunity and Inflammation - Guest Editor: Hajime Karasuyama

Philipp Starkl and Thomas Marichal contributed equally to this work.

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Mukai, K., Tsai, M., Starkl, P. et al. IgE and mast cells in host defense against parasites and venoms. Semin Immunopathol 38, 581–603 (2016). https://doi.org/10.1007/s00281-016-0565-1

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