ArticleJournal of immunology (Baltimore, Md. : 1950)1999
Fas-mediated suicide of tumor-reactive T cells following activation by specific tumor: selective rescue by caspase inhibition.
Article in Journal of immunology (Baltimore, Md. : 1950), 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 123 citations in OpenAlex.
- N-acetyl cysteine protects anti-melanoma cytotoxic T cells from exhaustion induced by rapid expansion via the downmodulation of Foxo1 in an Akt-dependent manner.Cancer immunology, immunotherapy : CII · 2018Article
- Effector function of CTLs is increased by irradiated colorectal tumor cells that modulate OX-40L and 4-1BBL and is reversed following dual blockade.BMC research notes · 2016Article
- Immunotherapy for solid tumors--a review for surgeons.The Journal of surgical research · 2014Review
- Turning T cells on: epigenetically enhanced expression of effector T-cell costimulatory molecules on irradiated human tumor cells.Journal for immunotherapy of cancer · 2013Article
- Activation-induced cell death of memory CD8+ T cells from pleural effusion of lung cancer patients is mediated by the type II Fas-induced apoptotic pathway.Cancer immunology, immunotherapy : CII · 2012Article
- Immunological responses in cancer patients after vaccination with the therapeutic telomerase-specific vaccine Vx-001.Cancer immunology, immunotherapy : CII · 2012Article
- Tumor-induced CD8+ T-cell dysfunction in lung cancer patients.Clinical & developmental immunology · 2012Review
- Targeting T cells with bispecific antibodies for cancer therapy.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2011Review
- Kainate-mediated excitotoxicity induces neuronal death in the rat spinal cord in vitro via a PARP-1 dependent cell death pathway (Parthanatos).Cellular and molecular neurobiology · 2010Article
- Article
- Tumor escape mechanisms in prostate cancer.Cancer immunology, immunotherapy : CII · 2007Review
- Flow cytometric analysis of Th1 and Th2 cytokines in PBMCs as a parameter of immunological dysfunction in patients of superficial transitional cell carcinoma of bladder.Cancer immunology, immunotherapy : CII · 2006Article
- FASL -844C polymorphism is associated with increased activation-induced T cell death and risk of cervical cancer.The Journal of experimental medicine · 2005Article
- Immunologic aspect of ovarian cancer and p53 as tumor antigen.Journal of translational medicine · 2005Article
- Role of cytokines in promoting immune escape of FasL-expressing human colon cancer cells.World journal of gastroenterology · 2005Article
- Effective immunotherapy against cancer: a question of overcoming immune suppression and immune escape?Cancer immunology, immunotherapy : CII · 2004Review
- Tumour-induced apoptosis in human mesothelial cells: a mechanism of peritoneal invasion by Fas Ligand/Fas interaction.British journal of cancer · 2004Article
- Article
- CD95 (Fas/APO-1)/CD95L in the gastrointestinal tract: fictions and facts.Virchows Archiv : an international journal of pathology · 2003Review
- Natural selection of tumor variants in the generation of "tumor escape" phenotypes.Nature immunology · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
CD8+ T lymphocytes that specifically recognize tumor cells can be isolated and expanded ex vivo. While the lytic properties of these cells have been well described, their fate upon encounter with cognate tumor is not known. We performed reverse 51Cr release assays in which the lymphocyte effectors rather than the tumor cell targets were radioactively labeled. We found that melanoma tumor cells caused the apoptotic death of tumor-specific T cells only upon specific MHC class I-restricted recognition. This death was entirely blockable by the addition of an Ab directed against the Fas death receptor (APO-1, CD95). Contrary to the prevailing view that tumor cells cause the death of anti-tumor T cells by expressing Fas ligand (FasL), our data suggested that FasL was instead expressed by T lymphocytes upon activation. While the tumor cells did not express FasL by any measure (including RT-PCR), functional FasL (as well as FasL mRNA) was consistently found on activated anti-tumor T cells. We could successfully block the activation-induced cell death with z-VAD-fmk, a tripeptide inhibitor of IL-1 beta-converting enzyme homologues, or with anti-Fas mAbs. Most importantly, these interventions did not inhibit T cell recognition as measured by IFN-gamma release, nor did they adversely affect the specific lysis of tumor cell targets. These results imply that Fas-mediated activation-induced cell death could be a limiting factor in the in vivo efficacy of adoptive transfer of class I-restricted CD8+ T cells and provide a means of potentially enhancing their growth in vitro as well as their function in vivo.
Indexed as
Identifiers
10092779PMC2239009W2135400695What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.