与昆虫、甲壳类、寄生虫和真菌相关的抗原，构成与人类的过敏和哮喘相关环境抗原的相当大的一部分。然而，将这些广泛分布的抗原联系起来的共同元素却仍然不知道。角素（chitin）也许是一大罪魁祸首。它是自然界第二种最丰富的聚合物，为无数细胞壁和刚性外骨骼提供渗透稳定性和张力。现在，Reese等人发现，用角素处理过的小鼠会产生过敏反应，特征是表达先天免疫细胞的白介素-4的积聚。用几丁质酶（或称甲壳质酶、壳多糖酶）处理后，这种反应会消失。在角素含量较高的环境（如甲壳类动物加工厂）中工作的人哮喘发病率较高，说明这一通道在人类过敏疾病的发病中也可能扮演一个角色。
英文原文：
Nature 447, 92-96 (3 May 2007) | doi:10.1038/nature05746; Received 30 January 2007; Accepted 13 March 2007; Published online 22 April 2007
Chitin induces accumulation in tissue of innate immune cells associated with allergy
Tiffany A. Reese1, Hong-Erh Liang1, Andrew M. Tager2, Andrew D. Luster2, Nico Van Rooijen3, David Voehringer1,4 & Richard M. Locksley1
Howard Hughes Medical Institute, Departments of Medicine and Microbiology/Immunology, University of California San Francisco, San Francisco, California 94143-0795, USA
Division of Rheumatology, Allergy and Immunology, Centre for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
Department of Molecular Cell Biology, Vrije Universiteit, 1091 BT, Amsterdam, The Netherlands
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).
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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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