Chitinase-like proteins promote IL-17-mediated neutrophilia in a tradeoff between nematode killing and host damage.

Tara Sutherland, Nicola Logan, Dominik Ruckerl, Alison A Humbles, Stuart Allan, Venizelos Papayannopoulos, Brigitta Stockinger, Rick M Maizels, Judith Allen

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157 Citations (Scopus)


Enzymatically inactive chitinase-like proteins (CLPs) such as BRP-39, Ym1 and Ym2 are established markers of immune activation and pathology, yet their functions are essentially unknown. We found that Ym1 and Ym2 induced the accumulation of neutrophils through the expansion of γδ T cell populations that produced interleukin 17 (IL-17). While BRP-39 did not influence neutrophilia, it was required for IL-17 production in γδ T cells, which suggested that regulation of IL-17 is an inherent feature of mouse CLPs. Analysis of a nematode infection model, in which the parasite migrates through the lungs, revealed that the IL-17 and neutrophilic inflammation induced by Ym1 limited parasite survival but at the cost of enhanced lung injury. Our studies describe effector functions of CLPs consistent with innate host defense traits of the chitinase family.
Original languageEnglish
Pages (from-to)1116-1125
Number of pages10
JournalNature Immunology
Issue number12
Publication statusPublished - 19 Oct 2014

Bibliographical note

We thank S. Duncan and Y. Harcus for technical assistance and R. Zamoyska for discussions. Supported by the Medical Research Council United Kingdom (MRC-UK MR/J001929/1, MR/K01207X/1 and U117512792 to B.S., and MC_UP_1202/13 for V.P.) and Asthma UK (06/057 & 10/040), with support from the Wellcome Trust funded Centre for Immunity, Infection and Evolution. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript


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