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Impact of FASL-induced apoptosis in the elimination of tumor cells by NK cells.

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Affiliations

  • 1. Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, S-141 86 Stockholm, Sweden.
      Authors
    • Screpanti V 1
    (1 author)

Molecular Immunology, 01 Feb 2005, 42(4):495-499
https://doi.org/10.1016/j.molimm.2004.07.033 PMID: 15607805 

Review

Abstract 

The cytotoxic effector functions of NK cells are important for enabling the immune system to cope efficiently with infection and malignancy. Two major mechanisms of cytotoxicity are perforin/granzyme- and death receptor-mediated (e.g., FASL- or TRAIL-mediated) induction of cell death. Many studies, including studies in perforin-deficient animals, have led to the conclusion that perforin/granzyme-mediated induction of cell death is a principal pathway used by NK cells to eliminate virus-infected or transformed cells. However, death receptor-mediated apoptosis may also contribute to NK cell-mediated cytotoxicity, as revealed by more recent reports. In the present paper, we have reviewed current data on death receptor-mediated tumor cell apoptosis by NK cells with a particular emphasis on the role of NK cell FASL in the RMA/RMA-S tumor model.

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Read article at publisher's site: https://doi.org/10.1016/j.molimm.2004.07.033

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