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Blood, 1 July 2002, Vol. 100, No. 1, pp. 327-333
TRANSPLANTATION
Enhancement of G-CSF-induced stem cell mobilization by
antibodies against the  2 integrins LFA-1 and Mac-1
Gerjo A. Velders,
Johannes
F. M. Pruijt,
Perry Verzaal,
Ronald van Os,
Yvette van Kooyk,
Carl G. Figdor,
Evert-Jan F. M. de
Kruijf,
Roel Willemze, and
Willem E. Fibbe
From the Laboratory of Experimental Hematology,
Department of Hematology, Leiden University Medical Center; and
Department of Tumor Immunology, University of Nijmegen; both of The
Netherlands.
The  2 integrins leukocyte function antigen-1 (LFA-1, CD11a) and
macrophage antigen-1 (Mac-1, CD11b) have been reported to play a role
in the attachment of CD34+ cells to stromal cells in the
bone marrow. When administered prior to interleukin-8 (IL-8),
anti-LFA-1 antibodies completely prevent the IL-8-induced
mobilization of hematopoietic stem cells in mice. Here, we studied the
role of anti-2 integrin antibodies in granulocyte colony-stimulating
factor (G-CSF)-induced mobilization of hematopoietic progenitor cells.
Administration of antibodies against the  chain of LFA-1 or against
the chain of Mac-1 followed by daily injections of G-CSF for more
than 1 day resulted in a significant enhancement of mobilization of
hematopoietic progenitor cells when compared with mobilization induced
by G-CSF alone. Also, the number of late (day 28) cobblestone
area-forming cells in vitro was significantly higher after
mobilization with anti-LFA-1 antibodies followed by 5 µg G-CSF for
5 days than with G-CSF alone (119 ± 34 days vs 17 ± 14
days), indicating mobilization of repopulating stem cells. Pretreatment
with blocking antibodies to intercellular adhesion molecule-1 (ICAM-1;
CD54), a ligand of LFA-1 and Mac-1, did not result in an effect on
G-CSF-induced mobilization, suggesting that the enhancing effect
required an interaction of the 2 integrins and one of their other
ligands. Enhancement of mobilization was not observed in
LFA-1-deficient (CD11a) mice, indicating that activated cells
expressing LFA-1 mediate the synergistic effect, rather than
LFA-1-mediated adhesion.
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