Neuro-immune crosstalk and allergic inflammation
Hiroki Kabata and David Artis
Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, New York, USA.
Address correspondence to: David Artis, Weill Cornell Medicine, Cornell University, Joan and Sanford I. Weill Department of Medicine, Belfer Research Building, Room 724 (box 210), 413 East 69th Street, New York, New York 10021, USA. Phone: 646.962.6291; Email: dartis@med.cornell.edu.
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Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, New York, USA.
Address correspondence to: David Artis, Weill Cornell Medicine, Cornell University, Joan and Sanford I. Weill Department of Medicine, Belfer Research Building, Room 724 (box 210), 413 East 69th Street, New York, New York 10021, USA. Phone: 646.962.6291; Email: dartis@med.cornell.edu.
Find articles by Artis, D. in: JCI | PubMed | Google Scholar
First published March 4, 2019 - More info
© 2019 American Society for Clinical Investigation
The neuronal and immune systems exhibit bidirectional interactions that play a critical role in tissue homeostasis, infection, and inflammation. Neuron-derived neuropeptides and neurotransmitters regulate immune cell functions, whereas inflammatory mediators produced by immune cells enhance neuronal activation. In recent years, accumulating evidence suggests that peripheral neurons and immune cells are colocalized and affect each other in local tissues. A variety of cytokines, inflammatory mediators, neuropeptides, and neurotransmitters appear to facilitate this crosstalk and positive-feedback loops between multiple types of immune cells and the central, peripheral, sympathetic, parasympathetic, and enteric nervous systems. In this Review, we discuss these recent findings regarding neuro-immune crosstalk that are uncovering molecular mechanisms that regulate inflammation. Finally, neuro-immune crosstalk has a key role in the pathophysiology of allergic diseases, and we present evidence indicating that neuro-immune interactions regulate asthma pathophysiology through both direct and indirect mechanisms.
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Copyright © 2019 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)