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Lookup NU author(s): Dr Lee Borthwick
This is the authors' accepted manuscript of an article that has been published in its final definitive form by Nature Publishing Group, 2016.
For re-use rights please refer to the publisher's terms and conditions.
Acidic mammalian chitinase (AMCase) is known to be induced by allergens and helminths, yet its role in immunity is unclear. Using AMCase-deficient mice, we show that AMCase deficiency reduced the number of group 2 innate lymphoid cells during allergen challenge but was not required for establishment of type 2 inflammation in the lung in response to allergens or helminths. In contrast, AMCase-deficient mice showed a profound defect in type 2 immunity following infection with the chitin-containing gastrointestinal nematodes Nippostrongylus brasiliensis and Heligmosomoides polygyrus bakeri. The impaired immunity was associated with reduced mucus production and decreased intestinal expression of the signature type 2 response genes Il13, Chil3, Retnlb, and Clca1. CD103(+) dendritic cells, which regulate T cell homing, were also reduced in mesenteric lymph nodes of infected AMCase-deficient mice. Thus, AMCase functions as a critical initiator of protective type 2 responses to intestinal nematodes but is largely dispensable for allergic responses in the lung.
Author(s): Vannella KM, Ramalingam TR, Hart KM, Prado RD, Sciurba J, Barron L, Borthwick LA, Smith AD, Mentink-Kane M, White S, Thompson RW, Cheever AW, Bock K, Moore I, Fitz LJ, Urban JF, Wynn TA
Publication type: Article
Publication status: Published
Journal: Nature Immunology
Year: 2016
Volume: 17
Issue: 5
Pages: 538-544
Print publication date: 01/05/2016
Online publication date: 04/04/2016
Acceptance date: 18/02/2016
Date deposited: 16/06/2016
ISSN (print): 1529-2908
ISSN (electronic): 1529-2916
Publisher: Nature Publishing Group
URL: http://dx.doi.org/10.1038/ni.3417
DOI: 10.1038/ni.3417
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