CD95L mediates tumor counterattack in vitro but induces neutrophil-independent tumor rejection in vivo
Many tumors express CD95L (CD178, FasL, APO-1L) and may thus kill tumor-infiltrating lymphocytes, a phenomenon called tumor counterattack. However, presently it is not clear whether tumor counterattack is a relevant immune escape mechanism. To characterize the effect of CD95L expression of tumor cel...
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| Main Authors: | , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
2005
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| In: |
International journal of cancer
Year: 2004, Volume: 113, Issue: 1, Pages: 78-87 |
| ISSN: | 1097-0215 |
| DOI: | 10.1002/ijc.20538 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1002/ijc.20538 Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.20538 
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| Author Notes: | Frederik H. Igney, Christian K. Behrens and Peter H. Krammer |
| Summary: | Many tumors express CD95L (CD178, FasL, APO-1L) and may thus kill tumor-infiltrating lymphocytes, a phenomenon called tumor counterattack. However, presently it is not clear whether tumor counterattack is a relevant immune escape mechanism. To characterize the effect of CD95L expression of tumor cells on tumor-specific T cells, we established an in vitro system with TCR tg T cells and a model tumor antigen. Preactivated antitumor T cells were able to kill CD95L− and CD95L+ tumor cells. CD95L+ tumor cells killed activated T cells in vitro and inhibited the expansion of cytotoxic antitumor T cells in mixed lymphocyte tumor reactions. In vivo CD95L expression led to delayed tumor growth or complete tumor rejection. Neutrophils were not responsible for the delayed growth of the CD95L+ tumors tested. In mice with neutrophils deficient for important cytotoxicity mechanisms (p47phox−/− or iNOS−/− mice), CD95L+ tumors grew similarly as in wild-type mice. Incidence and growth rate of CD95L+ tumors in mice injected with a neutrophil-depleting or an isotype control antibody was the same. In CD95-deficient lpr mice, tumor growth was not altered as compared to wild-type mice. Taken together, CD95L mediated tumor counterattack in vitro, but led to neutrophil-independent tumor rejection in vivo. |
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| Item Description: | First published: 25 August 2004 Gesehen am 04.03.2021 |
| Physical Description: | Online Resource |
| ISSN: | 1097-0215 |
| DOI: | 10.1002/ijc.20538 |