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Human Natural Killer Cytotoxic Factor (NKCF)

Relevance, Mode of Action, and Relationship to Other Cytotoxic Factors

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Leukolysins and Cancer

Part of the book series: Contemporary Biomedicine ((CB,volume 8))

Abstract

During the past few years, natural killer (NK) cells have attracted considerable attention because of their potential role in antitumor defenses in humans and animals (1). Recently, the cells responsible for NK activity in rodents and humans have been shown to be a subset of lymphoid cells termed large granular lymphocytes (LGL) (2,3). The mechanism of their lytic activity is still not thoroughly understood, however. Studies of the effects of metabolic inhibitors on NK activity support the stimulation-secretion model originally postulated (4,5) to explain the mechanism of killing by cytotoxic T lymphocytes (CTL) (6). In addition, Wright and Bonavida (7) have recently described a soluble factor that is produced during the interaction of mouse spleen cells and human peripheral blood lymphocytes (7–10) and that selectively lyses NK-susceptible target cells. They termed this NK cytotoxic factor (NKCF). Although several lines of correlative evidence suggest a role for NKCF in the mechanism of NK cellmediated cytolysis, a variety of important issues still remain to be settled. In the present report, NKCF was utilized in an attempt to dissect the various steps that have been postulated to be involved in NK cell-mediated lysis. Studies were performed to examine agents that have been previously demonstrated to inhibit LGL-mediated cytolysis and their effect on NKCF production by LGL and NKCF lysis of tumor target cells.

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© 1988 The Humana Press Inc.

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Ortaldo, J.R. (1988). Human Natural Killer Cytotoxic Factor (NKCF). In: Ransom, J.H., Ortaldo, J.R. (eds) Leukolysins and Cancer. Contemporary Biomedicine, vol 8. Humana Press. https://doi.org/10.1007/978-1-4612-4586-5_8

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  • DOI: https://doi.org/10.1007/978-1-4612-4586-5_8

  • Publisher Name: Humana Press

  • Print ISBN: 978-1-4612-8938-8

  • Online ISBN: 978-1-4612-4586-5

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