We are analyzing https://link.springer.com/article/10.1007/s002620050505.

Title:
T cell–tumor cell: a fatal interaction? | Cancer Immunology, Immunotherapy
Description:
Fas (Apo-1/CD95) is a cell-surface protein that is responsible for initiating a cascade of proteases (caspases) culminating in apoptotic cell death in a variety of cell types. The function of the Fas/FasL system in the dampening of immune responses to infectious agents through the autocrine deletion of activated T cells has been well documented. More recently, it has been proposed that tumor cells express FasL, presumably to avoid immune detection. In this review, we focus on the role of the interaction of Fas and FasL in the modulation of antitumor responses. We critically examine the evidence that FasL is expressed by tumor cells and explore alternative explanations for the observed phenomena in vitro and in vivo. By reviewing data that we have generated in our laboratory as well as reports from the literature, we will argue that the Fas/FasL system is a generalized mechanism used in an autocrine fashion to regulate cell survival and expansion in response to environmental and cellular cues. We propose that FasL expression by tumor cells, when present, is indicative of a perturbed balance in the control of proliferation while “immune privilege” is established by “suicide” of activated antitumor T cells, a form of activation-induced cell death.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

article, cell, access, privacy, cookies, content, cancer, cells, fasl, data, information, publish, research, search, immune, log, journal, immunology, immunotherapy, interaction, chappell, restifo, explore, fas, death, tumor, apoptosis, open, discover, usa, springer, function, optional, personal, parties, policy, find, track, celltumor, fatal, review, september, cite, dale, nicholas, fasfasl, system, responses, autocrine, activated,

Topics {✒️}

activation-induced cell death article cancer immunology cell–tumor cell related subjects apoptotic cell death month download article/chapter explore alternative explanations cell-surface protein regulate cell survival fasl expression september 1998 volume 47 full article pdf privacy choices/manage cookies check access instant access immunotherapy article avoid immune detection cell types european economic area fas/fasl system conditions privacy policy apoptosis human fas ligand accepting optional cookies national institutes journal finder publish article chappell article log tumor cells tumor-infiltrating immunotherapy aims generalized mechanism article cite privacy policy information personal data immune responses �immune privilege” books a optional cookies manage preferences subscription content similar content essential cookies cookies skip data protection reviewing data institution subscribe journal publish usage analysis

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T cell–tumor cell: a fatal interaction?
T cell–tumor cell: a fatal interaction?

Schema {🗺️}

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         description: Fas (Apo-1/CD95) is a cell-surface protein that is responsible for initiating a cascade of proteases (caspases) culminating in apoptotic cell death in a variety of cell types. The function of the Fas/FasL system in the dampening of immune responses to infectious agents through the autocrine deletion of activated T cells has been well documented. More recently, it has been proposed that tumor cells express FasL, presumably to avoid immune detection. In this review, we focus on the role of the interaction of Fas and FasL in the modulation of antitumor responses. We critically examine the evidence that FasL is expressed by tumor cells and explore alternative explanations for the observed phenomena in vitro and in vivo. By reviewing data that we have generated in our laboratory as well as reports from the literature, we will argue that the Fas/FasL system is a generalized mechanism used in an autocrine fashion to regulate cell survival and expansion in response to environmental and cellular cues. We propose that FasL expression by tumor cells, when present, is indicative of a perturbed balance in the control of proliferation while “immune privilege” is established by “suicide” of activated antitumor T cells, a form of activation-induced cell death.
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