IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses

Changchun Chen, Eisuke Itakura, Geoffrey M. Nelson, Ming Sheng, Patrick Laurent, Lorenz A. Fenk, Rebecca A. Butcher, Ramanujan S. Hegde and Mario de Bono ()
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Changchun Chen: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Eisuke Itakura: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Geoffrey M. Nelson: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Ming Sheng: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Patrick Laurent: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Lorenz A. Fenk: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Rebecca A. Butcher: University of Florida
Ramanujan S. Hegde: MRC Laboratory of Molecular Biology, Francis Crick Avenue
Mario de Bono: MRC Laboratory of Molecular Biology, Francis Crick Avenue

Nature, 2017, vol. 542, issue 7639, 43-48

Abstract: Abstract Interleukin-17 (IL-17) is a major pro-inflammatory cytokine: it mediates responses to pathogens or tissue damage, and drives autoimmune diseases. Little is known about its role in the nervous system. Here we show that IL-17 has neuromodulator-like properties in Caenorhabditis elegans. IL-17 can act directly on neurons to alter their response properties and contribution to behaviour. Using unbiased genetic screens, we delineate an IL-17 signalling pathway and show that it acts in the RMG hub interneurons. Disrupting IL-17 signalling reduces RMG responsiveness to input from oxygen sensors, and renders sustained escape from 21% oxygen transient and contingent on additional stimuli. Over-activating IL-17 receptors abnormally heightens responses to 21% oxygen in RMG neurons and whole animals. IL-17 deficiency can be bypassed by optogenetic stimulation of RMG. Inducing IL-17 expression in adults can rescue mutant defects within 6 h. These findings reveal a non-immunological role of IL-17 modulating circuit function and behaviour.

Date: 2017
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DOI: 10.1038/nature20818

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