Tiazofurin Induces a Down-Modulation of ICAM-1 Expression on K562 Target Cells Impairing NK Adhesion and Killing

Loris Zamai, Giorgio Zauli, Alberto Bavelloni, Sandra Marmiroli, Amelia Cataldi, George Weber, Marco Vitale

Research output: Contribution to journalArticle

Abstract

Tiazofurin treatment of K562 leukemia cells in vitro depletes the metabolites of the guanylate biosynthetic pathway, inducing erythroid differentiation, that, in turn, alters the pheuotypic profile. As a consequence, K562 cells possibly modify their interaction with immune cells. Here we describe the binding and killing activity of peripheral blood NK cells against differentiating K562 cells and the correlation between their altered binding capacity and ICAM-1 expression levels in differentiating K562 cells. We found that decreased percentages of NK (and T) cells were bound to differentiating K562 cells generating a decreased cytotoxic activity. This corresponded to decreased expression of ICAM-1, as detected by FACS analysis and Western blot. Erythroid differentiation, binding and killing reduction, and ICAM-1 down-modulation were completely abrogated by guanosine treatment. Tiazofurin causes a decrease in lymphocyte recognition and binding to K562 target cells. This can be ascribed to the down-modulation of ICAM-1 expression on target cells, which, therefore, can escape killing, acquiring a selective survival advantage.

Original languageEnglish
Pages (from-to)100-104
Number of pages5
JournalCellular Immunology
Volume164
Issue number1
DOIs
Publication statusPublished - Aug 1995

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

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