Chitin induces accumulation in tissue of innate immune cells associated with allergy

Tiffany A. Reese, Hong-Erh Liang, Andrew M. Tager, Andrew D. Luster, Nico Van Rooijen, David Voehringer and Richard M. Locksley ()
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Tiffany A. Reese: Howard Hughes Medical Institute, University of California San Francisco, San Francisco, California 94143-0795, USA
Hong-Erh Liang: Howard Hughes Medical Institute, University of California San Francisco, San Francisco, California 94143-0795, USA
Andrew M. Tager: Allergy and Immunology, Centre for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Andrew D. Luster: Allergy and Immunology, Centre for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Nico Van Rooijen: Vrije Universiteit, 1091 BT, Amsterdam, The Netherlands
David Voehringer: Howard Hughes Medical Institute, University of California San Francisco, San Francisco, California 94143-0795, USA
Richard M. Locksley: Howard Hughes Medical Institute, University of California San Francisco, San Francisco, California 94143-0795, USA

Nature, 2007, vol. 447, issue 7140, 92-96

Abstract: Chitin allergy Antigens associated with insects, crustacea, helminths and fungi make up a considerable proportion of the environmental antigens associated with allergies and asthma in humans. Nonetheless, the common elements that link these widely distributed entities remain unknown. A major culprit might be chitin. Chitin is the second most abundant polymer in nature, providing the osmotic stability and tensile strength to countless cell walls and rigid exoskeletons. Reese et al. have now found that mice treated with chitin develop an allergic response, characterized by a build-up of interleukin-4 expressing innate immune cells. Treatment with a chitinase enzyme abolishes the response. Occupations associated with high environmental chitin levels, such as shellfish processors, are prone to high incidences of asthma, suggesting that this pathway may play a role in human allergic disease.

Date: 2007
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DOI: 10.1038/nature05746

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