Tiazofurin induces a down-modulation of ICAM-1 expression on K562 target cells impairing NK adhesion and killing.

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 phenotypic 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.

journal_name

Cell Immunol

journal_title

Cellular immunology

authors

Zamai L,Zauli G,Bavelloni A,Marmiroli S,Cataldi A,Weber G,Vitale M

doi

10.1006/cimm.1995.1147

subject

Has Abstract

pub_date

1995-08-01 00:00:00

pages

100-4

issue

1

eissn

0008-8749

issn

1090-2163

pii

S0008-8749(85)71147-1

journal_volume

164

pub_type

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