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Cell Rep. 2017 Aug 15;20(7):1667-1680. doi: 10.1016/j.celrep.2017.07.063.

The IL-17F/IL-17RC Axis Promotes Respiratory Allergy in the Proximal Airways.

Author information

1
Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy.
2
European Institute for Research in Cystic Fibrosis, San Raffaele Scientific Institute, Milan, Italy.
3
Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital Brno, Czech Republic.
4
European Institute for Research in Cystic Fibrosis, San Raffaele Scientific Institute, Milan, Italy; Department of Health Sciences, University of Eastern Piedmont, Novara, Italy.
5
Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy. Electronic address: teresa.zelante@unipg.it.

Abstract

The interleukin 17 (IL-17) cytokine and receptor family is central to antimicrobial resistance and inflammation in the lung. Mice lacking IL-17A, IL-17F, or the IL-17RA subunit were compared with wild-type mice for susceptibility to airway inflammation in models of infection and allergy. Signaling through IL-17RA was required for efficient microbial clearance and prevention of allergy; in the absence of IL-17RA, signaling through IL-17RC on epithelial cells, predominantly by IL-17F, significantly exacerbated lower airway Aspergillus or Pseudomonas infection and allergic airway inflammation. In contrast, following infection with the upper respiratory pathogen Staphylococcus aureus, the IL-17F/IL-17RC axis mediated protection. Thus, IL-17A and IL-17F exert distinct biological effects during pulmonary infection; the IL-17F/IL-17RC signaling axis has the potential to significantly worsen pathogen-associated inflammation of the lower respiratory tract in particular, and should be investigated further as a therapeutic target for treating pathological inflammation in the lung.

KEYWORDS:

ABPA; IL-17F/IL-17RC axis; Th17 immunity; allergy; respiratory infections

PMID:
28813677
DOI:
10.1016/j.celrep.2017.07.063
[Indexed for MEDLINE]
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