| Literature DB >> 29070673 |
Jarod A Zepp1,2, Junjie Zhao1,2, Caini Liu1, Katazyna Bulek1, Ling Wu1,3, Xing Chen1, Yujun Hao4, Zhenghe Wang4, Xinxin Wang5,6, Wenjun Ouyang7, Matthew F Kalady8, Julie Carman9, Wen-Pin Yang9, Jun Zhu9, Clare Blackburn10, Yina H Huang5,6, Thomas A Hamilton1,2, Bing Su11,12, Xiaoxia Li13,2,3.
Abstract
This study identifies a novel mechanism linking IL-17A with colon tissue repair and tumor development. Abrogation of IL-17A signaling in mice attenuated tissue repair of dextran sulfate sodium (DSS)-induced damage in colon epithelium and markedly reduced tumor development in an azoxymethane/DSS model of colitis-associated cancer. A novel IL-17A target gene, PLET1 (a progenitor cell marker involved in wound healing), was highly induced in DSS-treated colon tissues and tumors in an IL-17RC-dependent manner. PLET1 expression was induced in LGR5+ colon epithelial cells after DSS treatment. LGR5+PLET1+ marks a highly proliferative cell population with enhanced expression of IL-17A target genes. PLET1 deficiency impaired tissue repair of DSS-induced damage in colon epithelium and reduced tumor formation in an azoxymethane/DSS model of colitis-associated cancer. Our results suggest that IL-17A-induced PLET1 expression contributes to tissue repair and colon tumorigenesis.Entities:
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Year: 2017 PMID： 29070673 PMCID： PMC5771493 DOI： 10.4049/jimmunol.1601540
Source DB: PubMed Journal: J Immunol ISSN： 0022-1767 Impact factor: 5.422