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evi
2,*,
i
*
Department of Physiology and
Croatian Institute for Brain Research and Basic Medical Sciences, Zagreb University School of Medicine, Zagreb, Croatia; and
Division of Endocrinology and Metabolism, Department of Medicine, University of Connecticut Health Center, Farmington, CT 06030
To investigate the role of T lymphocytes in osteoclastogenesis, we
performed in vivo depletion of CD4 and/or CD8 T lymphocyte subsets and
evaluated in vitro osteoclast-like cell (OCL) formation. T lymphocyte
depletion (TLD) with mAbs was confirmed 24 h later by flow
cytometry. OCL formation was stimulated with 1,25-dihydroxyvitamin
D3 (1,25-(OH)2D3) in bone marrow
and with recombinant mouse (rm) receptor activator of NF-
B ligand
(RANK-L) and rmM-CSF in bone marrow and spleen cell cultures. OCL
formation was up to 2-fold greater in
1,25-(OH)2D3-stimulated bone marrow cultures
from TLD mice than in those from intact mice. In contrast, TLD did not
alter OCL formation in bone marrow or spleen cell cultures that were
stimulated with rmRANK-L and rmM-CSF. The effects of TLD seemed to be
mediated by enhanced PG synthesis, because the PGE2
concentration in the medium of
1,25-(OH)2D3-stimulated bone marrow cultures
from TLD mice was 5-fold higher than that in cultures from intact mice,
and indomethacin treatment abolished the stimulatory effect of TLD on
OCL formation. There was a 2-fold increase in RANK-L expression and an
almost complete suppression of osteoprotegerin expression in
1,25-(OH)2D3-stimulated bone marrow cultures
from TLD mice compared with those from intact mice. Although there was
a small (20%) increase in IL-1
expression in
1,25-(OH)2D3-stimulated bone marrow cultures
from TLD mice, TLD in mice lacking type I IL-1R and wild-type mice
produced similar effects on OCL formation. Our data demonstrate that
TLD up-regulates OCL formation in vitro by increasing PG production,
which, in turn, produces reciprocal changes in RANK-L and
osteoprotegerin expression. These results suggest that T lymphocytes
influence osteoclastogenesis by altering bone marrow stromal cell
function.
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