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  • American Society of Hematology  (4)
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  • American Society of Hematology  (4)
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  • 1
    Online Resource
    Online Resource
    Role of Spontaneous and Interleukin-2–Induced Natural Killer Cell Activity in the Cytotoxicity and Rejection of Fas+and Fas− Tumor Cells
    American Society of Hematology ; 1998
    In:  Blood Vol. 92, No. 11 ( 1998-12-01), p. 4248-4255
    Details
    In: Blood, American Society of Hematology, Vol. 92, No. 11 ( 1998-12-01), p. 4248-4255
    Abstract: In the current study, we investigated whether the naive, poly I:C or interleukin-2 (IL-2)–induced natural killer (NK)/lymphokine-activated killer (LAK) cells use perforin and/or Fas ligand (FasL) to mediated cytotoxicity. We correlated these findings with the ability of mice to reject syngeneic Fas+ and Fas− tumor cells either spontaneously or after IL-2 treatment. The spontaneous NK-cell–mediated cytotoxicity was primarily perforin based, whereas the poly I:C and IL-2–induced NK/LAK activity was both FasL and perforin dependent. L1210 Fas+ tumor targets were more sensitive than L1210 Fas− targets to poly I:C and IL-2–induced cytotoxicity in wild-type, gld/gld, and perforin knockout mice. When L1210 Fas+ and Fas– tumor cells were injected subcutaneously (sc) or intraperitoneally into syngeneic mice, Fas− tumor cells caused mortality earlier than Fas+ tumor cells. Also, approximately 20% of the mice injected sc with L1210 Fas+ tumor cells survived the challenge( 〉 60 days), whereas all mice injected similarly with L1210 Fas− tumor cells died. When immunotherapy using IL-2 (10,000 U, three times/d for a week, followed by once/d for an additional week) was attempted in mice injected sc with tumor cells, IL-2 treatment was very effective against mice bearing L1210 Fas+ (40% survival) but not L1210 Fas− (0% survival) tumors. These data correlated with the finding that the LAK cells from IL-2–injected mice caused increased cytotoxicity against L1210 Fas+ when compared with L1210 Fas− targets. Also, L1210 Fas+tumor-bearing mice showed increased tumor-specific cytotoxic T lymphocyte (CTL) activity when compared with those bearing L1210 Fas− tumor cells. Together our studies show for the first time that expression of Fas on tumor targets makes them more immunogenic as well as susceptible to CTL- and IL-2–induced LAK activity. The Fas+ tumor cells are also more responsive to immunotherapy with IL-2.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V92.11.4248.423k20_4248_4255
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1998
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Fas-Fas Ligand–Based Interactions Between Tumor Cells and Tumor-Specific Cytotoxic T Lymphocytes: A Lethal Two-Way Street
    American Society of Hematology ; 1997
    In:  Blood Vol. 90, No. 5 ( 1997-09-01), p. 1952-1959
    Details
    In: Blood, American Society of Hematology, Vol. 90, No. 5 ( 1997-09-01), p. 1952-1959
    Abstract: In the current study, we investigated the repercussions of the interaction between tumor cells (LSA) and the tumor-specific cytotoxic T lymphocyte (CTL) (PE-9) when both expressed Fas and Fas ligand (FasL). The CTL clone, PE-9, expressed high levels of Fas and FasL upon activation through the T-cell receptor (TCR). Furthermore, the activated PE-9 cells used both perforin- and FasL-based pathways to kill Fas-positive (Fas+) LSA tumor cells. Interestingly, LSA tumor cells also constitutively expressed FasL but not perforin, and killed Fas+ PE-9 CTLs and Fas+ but not Fas-negative (Fas−) activated T cells and thymocytes, as detected using the JAM test. PE-9 CTLs, cultured for 24 hours in the presence of cell lysates of FasL-bearing LSA cells but not FasL-deficient P815 cells, exhibited significant apoptosis as detected using the TUNEL method. Moreover, another FasL+ T-cell lymphoma line, EL-4, induced apoptosis in Fas+ but not in Fas− T cells in a similar fashion. The current study demonstrates for the first time that not only can the tumor-specific CTL mediate Fas-based killing of tumor cells, but FasL+ tumor cells can kill the Fas+ tumor-specific CTL. Thus, the survival of the tumor or the host may depend on which cell can accomplish this task more efficiently. The current study also suggests that FasL-based killing of CTLs by specific tumor cells may constitute a major limiting factor in successful immunotherapy.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V90.5.1952
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1997
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Growth of FasL-bearing tumor cells in syngeneic murine host induces apoptosis and toxicity in Fas+ organs
    American Society of Hematology ; 2000
    In:  Blood Vol. 95, No. 6 ( 2000-03-15), p. 2111-2117
    Details
    In: Blood, American Society of Hematology, Vol. 95, No. 6 ( 2000-03-15), p. 2111-2117
    Abstract: In the current study, we investigated whether the growth of FasL-bearing tumor cells would induce apoptosis and toxicity in organs that express high level of Fas. Sera from C57BL/6 +/+(wild-type) mice injected with syngeneic FasL+ tumors, LSA, or EL-4, showed significantly higher levels of soluble FasL than that from the nontumor-bearing mice. Furthermore, the soluble FasL was functional inasmuch as the sera from tumor-bearing mice were able to induce apoptosis in Fas+ but not Fas−targets. Histopathologic studies and in situ TUNEL assay to detect apoptosis were carried out in C57BL/6 +/+(Fas+) or C57BL/6 lpr/lpr (Fas−) mice injected with syngeneic LSA and EL-4 tumor cells. The morphology of the liver and thymus from tumor bearing C57BL/6 +/+ mice showed marked damage and tissue destruction. In contrast, the liver and thymus from tumor-bearing C57BL/6 lpr/lpr mice showed minimal damage. Furthermore, the tumor-bearing C57BL/6 +/+, but not the C57BL/6 lpr/lpr, mice exhibited significant apoptosis in the liver and thymus. The FasL responsible for toxicity was tumor derived rather than host derived; tumor-bearing C57BL/6 gld/gld(FasL-defective) mice also exhibited significant apoptosis in the liver and thymus. Together, these data suggested that the in vivo growth of FasL-bearing tumor cells can induce significant apoptosis and toxicity in Fas+ tissues of the host. Such toxicity may be mediated by the soluble FasL produced by tumor cells.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V95.6.2111
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2000
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Role of Spontaneous and Interleukin-2–Induced Natural Killer Cell Activity in the Cytotoxicity and Rejection of Fas+and Fas− Tumor Cells
    American Society of Hematology ; 1998
    In:  Blood Vol. 92, No. 11 ( 1998-12-01), p. 4248-4255
    Details
    In: Blood, American Society of Hematology, Vol. 92, No. 11 ( 1998-12-01), p. 4248-4255
    Abstract: In the current study, we investigated whether the naive, poly I:C or interleukin-2 (IL-2)–induced natural killer (NK)/lymphokine-activated killer (LAK) cells use perforin and/or Fas ligand (FasL) to mediated cytotoxicity. We correlated these findings with the ability of mice to reject syngeneic Fas+ and Fas− tumor cells either spontaneously or after IL-2 treatment. The spontaneous NK-cell–mediated cytotoxicity was primarily perforin based, whereas the poly I:C and IL-2–induced NK/LAK activity was both FasL and perforin dependent. L1210 Fas+ tumor targets were more sensitive than L1210 Fas− targets to poly I:C and IL-2–induced cytotoxicity in wild-type, gld/gld, and perforin knockout mice. When L1210 Fas+ and Fas– tumor cells were injected subcutaneously (sc) or intraperitoneally into syngeneic mice, Fas− tumor cells caused mortality earlier than Fas+ tumor cells. Also, approximately 20% of the mice injected sc with L1210 Fas+ tumor cells survived the challenge( & gt;60 days), whereas all mice injected similarly with L1210 Fas− tumor cells died. When immunotherapy using IL-2 (10,000 U, three times/d for a week, followed by once/d for an additional week) was attempted in mice injected sc with tumor cells, IL-2 treatment was very effective against mice bearing L1210 Fas+ (40% survival) but not L1210 Fas− (0% survival) tumors. These data correlated with the finding that the LAK cells from IL-2–injected mice caused increased cytotoxicity against L1210 Fas+ when compared with L1210 Fas− targets. Also, L1210 Fas+tumor-bearing mice showed increased tumor-specific cytotoxic T lymphocyte (CTL) activity when compared with those bearing L1210 Fas− tumor cells. Together our studies show for the first time that expression of Fas on tumor targets makes them more immunogenic as well as susceptible to CTL- and IL-2–induced LAK activity. The Fas+ tumor cells are also more responsive to immunotherapy with IL-2.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V92.11.4248
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 1998
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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