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IL-17A-Induced PLET1 Expression Contributes to Tissue Repair and Colon Tumorigenesis

Jarod A Zepp1,2, Junjie Zhao1,2, Caini Liu1

  • 1Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195.

Journal of Immunology (Baltimore, Md. : 1950)
|October 27, 2017
PubMed

Insights

Interleukin-17A (IL-17A) signaling promotes colon tissue repair and tumor growth by inducing PLET1 expression in progenitor cells. Blocking IL-17A impaired healing and reduced colitis-associated cancer in mice.

Area of Science:

  • Gastroenterology and Hepatology
  • Immunology
  • Oncology

Background:

  • Interleukin-17A (IL-17A) is a cytokine implicated in inflammation and immunity.
  • The role of IL-17A in colon tissue repair and tumorigenesis remains incompletely understood.
  • Colitis-associated cancer models provide a platform to study inflammation-driven tumor development.

Purpose of the Study:

  • To elucidate the mechanism by which IL-17A influences colon tissue repair.
  • To investigate the role of IL-17A in the development of colitis-associated cancer.
  • To identify novel IL-17A target genes involved in colon epithelial cell function.

Main Methods:

  • Utilized mouse models with dextran sulfate sodium (DSS)-induced colon damage and azoxymethane/DSS-induced colitis-associated cancer.
  • Assessed the impact of IL-17A signaling abrogation on tissue repair and tumor development.
  • Investigated the expression of IL-17A target genes, including PLET1, in colon tissues and isolated LGR5+ epithelial cells.

Main Results:

  • Abrogation of IL-17A signaling attenuated DSS-induced colon tissue repair and reduced tumor formation.
  • PLET1, a novel IL-17A target gene and progenitor cell marker, was highly induced in DSS-treated tissues and tumors.
  • PLET1 expression was induced in LGR5+ colon epithelial cells, marking a proliferative population; PLET1 deficiency impaired repair and reduced tumorigenesis.

Conclusions:

  • IL-17A signaling promotes colon tissue repair and tumorigenesis through the induction of PLET1.
  • PLET1 plays a critical role in the proliferative response of colon epithelial cells during damage and cancer development.
  • Targeting the IL-17A-PLET1 axis may offer therapeutic strategies for inflammatory bowel disease and colon cancer.

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