Tumor counterattack: fact or fiction?
Cancer development relies on a variety of mechanisms that facilitate tumor growth despite the presence of a functioning immune system. Understanding these mechanisms may foster novel therapeutic approaches for oncology and organ transplantation. By expression of the apoptosis-inducing protein CD95L...
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| Main Authors: | , |
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| Format: | Article (Journal) Conference Paper |
| Language: | English |
| Published: |
12 May 2005
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| In: |
Cancer immunology immunotherapy
Year: 2005, Volume: 54, Issue: 11, Pages: 1127-1136 |
| ISSN: | 1432-0851 |
| DOI: | 10.1007/s00262-005-0680-7 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00262-005-0680-7 Verlag, lizenzpflichtig, Volltext: https://link.springer.com/article/10.1007%2Fs00262-005-0680-7 
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| Author Notes: | Frederik H. Igney, Peter H. Krammer |
MARC
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| 520 | |a Cancer development relies on a variety of mechanisms that facilitate tumor growth despite the presence of a functioning immune system. Understanding these mechanisms may foster novel therapeutic approaches for oncology and organ transplantation. By expression of the apoptosis-inducing protein CD95L (FasL, APO-1L, CD178), tumors may eliminate tumor-infiltrating lymphocytes and suppress anti-tumor immune responses, a phenomenon called “tumor counterattack”. On the one hand, preliminary evidence of tumor counterattack in human tumors exists, and CD95L expression can prevent T-cell responses in vitro. On the other hand, CD95L-expressing tumors are rapidly rejected and induce inflammation in mice. Here, we summarize and discuss the consequences of CD95L expression of tumor cells and its contribution to immune escape. | ||
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