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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
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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
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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.

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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.