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Constitutive Chemokine Production Results in Activation of Leukocyte
Function-Associated Antigen-1 on Adult T-Cell Leukemia Cells
Yoshiya Tanaka,
Shinichiro Mine,
Carl G. Figdor,
Atsushi Wake,
Hideyasu Hirano,
Junichi Tsukada,
Megumi Aso,
Koichi Fujii,
Kazuyoshi Saito,
Yvette van Kooyk, and
Sumiya Eto
From The First Department of Internal Medicine and the Department of
Biochemistry, University of Occupational and Environmental Health,
Japan, School of Medicine, Kitakyushu, Japan; the Department of Tumor
Immunology, University Hospital Nijmegen, Nijmegen, The Netherlands;
and the Department of Internal Medicine, Kokura Memorial Hospital,
Kitakyushu, Japan.
Adult T-cell leukemia (ATL) is characterized by massive infiltration
of circulating ATL cells into a variety of tissues, a finding often
associated with poor prognosis. Leukocyte migration from circulation
into tissue depends on integrin-mediated adhesion to endothelium, and
integrins are tightly regulated by several stimuli, such as
inflammatory chemokines. However, the exact mechanisms that enhance
adherence of leukemic cells to the endothelium and infiltration into
tissues remain to be fully understood. We investigated the mechanisms
of extravasation of leukemic cells using ATL cells and report the
following novel features of endogenous chemokine-induced adhesion of
ATL cells to the endothelium. ATL cells spontaneously adhered to
endothelial cells without exogenous stimulation. Integrin leukocyte
function-associated antigen-1 (LFA-1) on ATL cells was spontaneously
activated. ATL cells produced high amounts of chemokines, macrophage
inflammatory protein-1 (MIP-1), and MIP-1 . Adhesion of ATL
cells to endothelial cells and the expression of activated form of
LFA-1 were reduced by pretreatment with pertussis toxin, wortmannin, or
anti-MIP-1 and MIP-1 antibodies or transfection with antisense
of MIP-1 or MIP-1. Spontaneous polymerization of cytoskeletal
F-actin was observed in ATL cells, which was also inhibited by
pertussis toxin and wortmannin. We propose that ATL cells adhere to
endothelial cells through an adhesion cascade similar to normal
leukocytes and that the chemokines produced by ATL cells are involved
in triggering integrin LFA-1 through cytoskeletal rearrangement induced
by G-protein-dependent activation of phosphoinositide 3-kinases in an
autocrine manner. These events result in a strong adhesion of ATL cells
to the endothelium and spontaneous transendothelial migration.
Blood, Vol. 91 No. 10 (May 15), 1998:
pp. 3909-3919
© 1998 by The American Society of Hematology.
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