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Related Experiment Videos

Mechanisms responsible for signaling and functional defects

T E Reichert1, H Rabinowich, J T Johnson

  • 1University of Pittsburgh Cancer Institute, Pennsylvania 15213-2582, USA.

Journal of Immunotherapy (Hagerstown, Md. : 1997)
|July 22, 1998
PubMed
Summary

Lymphocytes in head and neck cancer patients show signaling defects and apoptosis, potentially induced by the tumor. These findings highlight tumor-mediated immune suppression in advanced cancer.

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Lymphocytes in advanced cancer patients exhibit signaling pathway abnormalities.
  • T cell receptor (TcR) and Fc gamma RIII signaling are often compromised.

Purpose of the Study:

  • To investigate signaling defects and apoptosis in lymphocytes from head and neck carcinoma (HNC) patients.
  • To determine if tumor cells induce lymphocyte apoptosis.

Main Methods:

  • Analysis of T lymphocytes from tumor-involved lymph nodes (LNLs) and peripheral blood (PBLs) of HNC patients.
  • Assessment of signaling molecule expression (zeta, epsilon chains, p56lck), Ca2+ flux, and kinase activity.
  • In situ analysis of patient biopsies, including TUNEL staining for apoptosis and FasL/Fas expression.

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  • In vitro co-incubation assays with HNC cell lines and normal lymphocytes.

    • Main Results:

    • HNC-associated lymphocytes displayed decreased TcR-zeta/epsilon expression, impaired Ca2+ flux, and altered kinase activity.
    • Apoptotic (TUNEL+) lymphocytes were abundant in HNC LNLs, with some co-expressing CD3-epsilon.
    • HNC cell lines and tumors expressed Fas Ligand (FasL), and LNLs expressed Fas.
    • Co-incubation experiments showed HNC cells induced lymphocyte apoptosis.

    Conclusions:

    • Signaling defects in HNC patients' lymphocytes are linked to tumor-induced apoptosis.
    • Tumor microenvironment, via FasL, may trigger lymphocyte apoptosis, contributing to immune evasion.