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Tumor counterattack: fact or fiction?

Frederik H Igney1, Peter H Krammer

  • 1Tumor Immunology Program, German Cancer Research Center (DKFZ), Heidelberg, Germany. frederik.igney@schering.de

Cancer Immunology, Immunotherapy : CII
|May 13, 2005
PubMed

Insights

Tumors use CD95L (FasL) to suppress anti-tumor immunity, a "tumor counterattack." However, CD95L expression also triggers inflammation and tumor rejection in mice, highlighting complex immune interactions.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Cancer immune evasion is critical for tumor growth.
  • Tumor cells employ mechanisms to suppress anti-tumor immune responses.
  • CD95L (FasL) is an apoptosis-inducing protein implicated in immune modulation.

Purpose of the Study:

  • To explore the dual role of CD95L expression in tumor immune escape.
  • To understand how CD95L contributes to the "tumor counterattack" phenomenon.
  • To review the consequences of CD95L expression on tumor-infiltrating lymphocytes and anti-tumor immunity.

Main Methods:

  • Literature review and synthesis of existing research on CD95L in cancer.
  • Analysis of in vitro studies demonstrating CD95L's effect on T-cell responses.
  • Examination of in vivo studies investigating CD95L-expressing tumors in mouse models.

Main Results:

  • CD95L expression by tumors can eliminate tumor-infiltrating lymphocytes, suppressing anti-tumor immunity.
  • In vitro, CD95L prevents T-cell responses.
  • Conversely, in mice, CD95L-expressing tumors are rapidly rejected and induce inflammation.

Conclusions:

  • CD95L exhibits paradoxical effects on anti-tumor immunity, acting as a double-edged sword.
  • Understanding CD95L's complex role is crucial for developing novel cancer therapies.
  • Further research is needed to reconcile conflicting findings and harness CD95L for therapeutic benefit.

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