NDLI: IL-17 suppresses immune effector functions in human papillomavirus-associated epithelial hyperplasia.

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IL-17 suppresses immune effector functions in human papillomavirus-associated epithelial hyperplasia.

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IL-17 suppresses immune effector functions in human papillomavirus-associated epithelial hyperplasia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Bridge, Jennifer A. Frazer, Ian H. Gosmann, Christina Blumenthal, Antje Mattarollo, Stephen R.
Description	Author Affiliation: Gosmann C ( University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Queensland 4102, Australia); Mattarollo SR ( University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Queensland 4102, Australia); Bridge JA ( University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Queensland 4102, Australia); Frazer IH ( University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Queensland 4102, Australia); Blumenthal A ( University of Queensland Diamantina Institute, Translational Research Institute, Brisbane, Queensland 4102, Australia)
Abstract	Persistent infection with high-risk human papillomaviruses (HPV) causes epithelial hyperplasia that can progress to cancer and is thought to depend on immunosuppressive mechanisms that prevent viral clearance by the host. IL-17 is a cytokine with diverse functions in host defense and in the pathology of autoimmune disorders, chronic inflammatory diseases, and cancer. We analyzed biopsies from patients with HPV-associated cervical intraepithelial neoplasia grade 2/3 and murine skin displaying HPV16 E7 protein-induced epithelial hyperplasia, which closely models hyperplasia in chronic HPV lesions. Expression of IL-17 and IL-23, a major inducer of IL-17, was elevated in both human HPV-infected and murine E7-expressing lesions. Using a skin-grafting model, we demonstrated that IL-17 in HPV16 E7 transgenic skin grafts inhibited effective host immune responses against the graft. IL-17 was produced by CD3(+) T cells, predominantly CD4(+) T cells in human, and CD4(+) and Î³Î´ T cells in mouse hyperplastic lesions. IL-23 and IL-1ß, but not IL-18, induced IL-17 production in E7 transgenic skin. Together, these findings demonstrate an immunosuppressive role for IL-17 in HPV-associated epithelial hyperplasia and suggest that blocking IL-17 in persistent viral infection may promote antiviral immunity and prevent progression to cancer.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400216
Journal	The Journal of Immunology
Issue Number	5
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cervical Intraepithelial Neoplasia Immunology Human Papillomavirus 16 Interleukin-17 Papillomavirus E7 Proteins Papillomavirus Infections Uterine Cervical Neoplasms Animals Cd4-positive T-lymphocytes Genetics Pathology Interleukin-1beta Interleukin-23 Mice Mice, Knockout Receptors, Antigen, T-cell, Gamma-delta Clinical Trial Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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