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Blood, 1 April 2001, Vol. 97, No. 7, pp. 2121-2129
NEOPLASIA
Endothelial cell activation by myeloblasts: molecular mechanisms
of leukostasis and leukemic cell dissemination
Anne Stucki,
Anne-Sophie Rivier,
Milica Gikic,
Natacha Monai,
Marc Schapira, and
Olivier Spertini
From the Division and Central Laboratory of Hematology,
Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Leukostasis and tissue infiltration by leukemic cells are
poorly understood life-threatening complications of acute leukemia. This study has tested the hypothesis that adhesion receptors and cytokines secreted by blast cells play central roles in these reactions. Immunophenotypic studies showed that acute myeloid leukemia
(AML) cells (n = 78) of the M0 to M5 subtypes of the French-American-British Cooperative Group expressed various amounts of
adhesion receptors, including CD11a, b, c/CD18, CD49d, e, f/CD29, CD54,
sCD15, and L-selectin. The presence of functional adhesion receptors
was evaluated using a nonstatic adhesion assay. The number of blast
cells attached to unactivated endothelium increased by 7 to 31 times
after a 6-hour exposure of endothelium to tumor necrosis factor
(TNF)- . Inhibition studies showed that multiple adhesion
receptors including L-selectin, E-selectin, VCAM-1, and CD11/CD18were involved in blast cell adhesion to TNF--activated endothelium. Leukemic cells were then cocultured at 37°C on
unactivated endothelial cell monolayers for time periods up to 24 hours. A time-dependent increase in the number of blasts attached to
the endothelium and a concomitant induction of ICAM-1, VCAM-1, and E-selectin were observed. Additional experiments revealed that endothelial cell activation by leukemic myeloblasts was caused by
cytokine secretion by blast cells, in particular TNF- and IL-1 ,
and direct contacts between adhesion receptors expressed by blast cells
and endothelial cells. Thus, leukemic cells have the ability to
generate conditions that promote their own adhesion to vascular
endothelium, a property that may have important implications for the
pathophysiology of leukostasis and tissue infiltration by leukemic
blast cells.
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