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Autoreactive T Cells and Chronic Fungal Infection Drive Esophageal Carcinogenesis

  1. Author:
    Zhu, Feng
    Willette Brown, Jami
    Song, Na-Young
    Lomada, Dakshayani
    Song, Yongmei
    Xue, Liyan
    Gray, Zane
    Zhao, Zitong
    Davis, Sean R
    Sun, David
    Zhang, Peilin
    Wu, Xiaolin
    Zhan, Qimin
    Richie, Ellen R
    Hu, Yinling

  2. Author Address

    Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA., Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Smithville, TX 78957, USA., State Key Laboratory of Molecular Oncology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China., Department of Pathology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China., Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA., Laboratory of Molecular Technology, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA., PZM Diagnostics, LLC, Charleston, WV 25314, USA., Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA. Electronic address: huy2@mail.nih.gov.,
    1. Year: 2017
    2. Date: Apr 12
  2. Journal: Cell Host & Microbe
    1. 21
    2. 4
    3. Pages: 478-493.e7
  4. Type of Article: Article
  5. Article Number: 478-493.e7
  6. ISSN: 1931-3128
  1. Abstract:

    Humans with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), a T cell-driven autoimmune disease caused by impaired central tolerance, are susceptible to chronic fungal infection and esophageal squamous cell carcinoma (ESCC). However, the relationship between autoreactive T cells and chronic fungal infection in ESCC development remains unclear. We find that kinase-dead Ikka knockin mice develop APECED-like phenotypes, including impaired central tolerance, autoreactive T cells, chronic fungal infection, and ESCCs expressing specific human ESCC markers. Using this model, we investigated the link between ESCC and fungal infection. Autoreactive CD4 T cells permit fungal infection and incite tissue injury and inflammation. Antifungal treatment or autoreactive CD4 T cell depletion rescues, whereas oral fungal administration promotes, ESCC development. Inhibition of inflammation or epidermal growth factor receptor (EGFR) activity decreases fungal burden. Fungal infection is highly associated with ESCCs in non-autoimmune human patients. Therefore, autoreactive T cells and chronic fungal infection, fostered by inflammation and epithelial injury, promote ESCC development. Published by Elsevier Inc.

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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.chom.2017.03.006
  3. PMID: 28407484
  4. View record in Web of Science®
  5. WOS: 000398896100009

Library Notes

  1. Fiscal Year: FY2016-2017
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