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    The Fas counterattack in vivo: apoptotic depletion of tumor-infiltrating lymphocytes associated with Fas ligand expression by human esophageal carcinoma.

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    Authors
    Bennett, M W
    O'Connell, J
    O'Sullivan, G C
    Brady, C
    Roche, D
    Collins, J K
    Shanahan, F
    Affiliation
    Department of Medicine, Cork University Hospital, Ireland.
    Issue Date
    2012-02-03T15:14:37Z
    MeSH
    Adenocarcinoma/*immunology/metabolism/pathology
    Antigens, CD95/*metabolism
    Apoptosis/*immunology
    Carcinoma, Squamous Cell/*immunology/metabolism/pathology
    Esophageal Neoplasms/*immunology/metabolism/pathology
    Fas Ligand Protein
    Humans
    Immunohistochemistry
    Ligands
    *Lymphocyte Depletion
    Lymphocytes, Tumor-Infiltrating/*immunology/pathology
    Membrane Glycoproteins/*biosynthesis
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    Citation
    J Immunol. 1998 Jun 1;160(11):5669-75.
    Journal
    Journal of immunology (Baltimore, Md. : 1950)
    URI
    http://hdl.handle.net/10147/209189
    PubMed ID
    9605174
    Abstract
    Various cancer cell lines express Fas ligand (FasL) and can kill lymphoid cells by Fas-mediated apoptosis in vitro. FasL expression has been demonstrated in several human malignancies in vivo. We sought to determine whether human esophageal carcinomas express FasL, and whether FasL expression is associated with increased apoptosis of tumor-infiltrating lymphocytes (TIL) in vivo, thereby contributing to the immune privilege of the tumor. Using in situ hybridization and immunohistochemistry, respectively, FasL mRNA and protein were colocalized to neoplastic esophageal epithelial cells in all esophageal carcinomas (squamous, n = 6; adenocarcinoma, n = 2). The Extent of FasL expression was variable, with both FasL-positive and FasL-negative neoplastic regions occurring within tumors. TIL were detected by immunohistochemical staining for the leukocyte common Ag, CD45. FasL expression was associated with a mean fourfold depletion of TIL when compared with FasL-negative areas within the same tumors (range 1.6- to 12-fold, n = 6,p < 0.05). Cell death of TIL was detected by dual staining of CD45 (immunohistochemistry) and DNA strand breaks (TUNEL, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling). There was a mean twofold increase in detectable cell death among TIL in FasL-positive areas compared with FasL-negative areas (range 1.6- to 2.4-fold, n = 6, p < 0.05). In conclusion, we demonstrate a statistically significant, quantitative reduction of TIL concomitant with significantly increased TIL apoptosis within FasL-expressing areas of esophageal tumors. Our findings suggest Fas-mediated apoptotic depletion of TIL in response to FasL expression by esophageal cancers, and provide the first direct, quantitative evidence to support the Fas counterattack as a mechanism of immune privilege in vivo in human cancer.
    Language
    eng
    ISSN
    0022-1767 (Print)
    0022-1767 (Linking)
    Collections
    Cork University Hospital

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