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Interferon-Mediated Regulation of the NK Target Structures of Normal or Lymphoma Cells

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Genetic and Phenotypic Markers of Tumors

Abstract

It is well know that Interferon (IF) has antitumor activity presumably based on different mechanisms of action. This class of compounds is capable of inhibiting the growth of neoplastic cells (1), and of enhancing the cytotoxic activity mediated by natural killer (NK) lymphocytes (2,3) and by activated macrophages (4). However, additional studies have shown that a decrease of the susceptibility of normal or neoplastic cells to NK attack occurs after in vitro pretreatment with IF (5,9). These findings indicate that IF interacts in some way with NK target structures (NKTS) on the cell membrane, modifying their expression, or affinity, for effector lymphocytes. A number of studies pointed out that IF pretreatment of the target produces a profound influence on the antigenic makeup of tumor cells, increasing the expression of histocompatibility antigens specified by the major histocompatibility complex (MHC) both in mice (10) and in humans (11, 13). More detailed studies showed that two subsets of class II Molecules specified by DR and DC loci of human MHC, are differentially susceptible to IF-mediated modulation. DC products were found to be increased more than DR products under the influence of gamma-IF (14). These observations prompted us to investigate whether IF would also be able to produce differential effects on distinct subsets of NKTS. Actually, the results of the present paper support this hypothesis and suggest that different cell lines contain non-cross reacting NKTS susceptible to IF-mediated modulation.

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© 1984 Plenum Press, New York

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Graziani, G., Grandori, C., Macchi, B., Pastore, S., Bonmassar, E., Bonmassar, A.G. (1984). Interferon-Mediated Regulation of the NK Target Structures of Normal or Lymphoma Cells. In: Aaronson, S.A., Frati, L., Verna, R. (eds) Genetic and Phenotypic Markers of Tumors. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4856-6_20

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  • DOI: https://doi.org/10.1007/978-1-4684-4856-6_20

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-4858-0

  • Online ISBN: 978-1-4684-4856-6

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