1. Howard Hughes Medical Institute, Departments of Medicine and Microbiology/Immunology, University of California San Francisco, San Francisco, California 94143-0795, USA
2. Division of Rheumatology, Allergy and Immunology, Centre for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
3. Department of Molecular Cell Biology, Vrije Universiteit, 1091 BT, Amsterdam, The Netherlands
4. Present address: Institute for Immunology, University of Munich, Munich D-80336, Germany.

Correspondence to: Richard M. Locksley¹ Correspondence and requests for materials should be addressed to R.M.L. (Email: locksley@medicine.ucsf.edu).

Abstract

Allergic and parasitic worm immunity is characterized by infiltration of tissues with interleukin (IL)-4- and IL-13-expressing cells, including T-helper-2 cells, eosinophils and basophils¹. Tissue macrophages assume a distinct phenotype, designated alternatively activated macrophages². Relatively little is known about the factors that trigger these host responses. Chitin, a widespread environmental biopolymer of N-acetyl--d-glucosamine, provides structural rigidity to fungi, crustaceans, helminths and insects³. Here, we show that chitin induces the accumulation in tissue of IL-4-expressing innate immune cells, including eosinophils and basophils, when given to mice. Tissue infiltration was unaffected by the absence of Toll-like-receptor-mediated lipopolysaccharide recognition but did not occur if the injected chitin was pre-treated with the IL-4- and IL-13-inducible mammalian chitinase, AMCase⁴, or if the chitin was injected into mice that overexpressed AMCase. Chitin mediated alternative macrophage activation in vivo and the production of leukotriene B₄, which was required for optimal immune cell recruitment. Chitin is a recognition element for tissue infiltration by innate cells implicated in allergic and helminth immunity and this process can be negatively regulated by a vertebrate chitinase.

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