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* Department of Immunology, Duke University Medical Center, Durham, NC 27710; and
Department of Genomics and Pathobiology, University of Alabama, Birmingham, AL 35294
L-selectin mediates the initial capture and subsequent rolling of
leukocytes along inflamed vascular endothelium and mediates lymphocyte
migration to peripheral lymphoid tissues. Leukocyte activation induces
rapid endoproteolytic cleavage of L-selectin from the cell surface,
generating soluble L-selectin (sL-selectin). Because human sL-selectin
retains ligand-binding activity in vitro, mouse sL-selectin and its in
vivo relevance were characterized. Comparable with humans, sL-selectin
was present in adult C57BL/6 mouse sera at 
1.7 µg/ml. Similar
levels of sL-selectin were present in sera from multiple mouse strains,
despite their pronounced differences in cell surface L-selectin
expression levels. Adhesion molecule-deficient mice prone to
spontaneous chronic inflammation and mice suffering from
leukemia/lymphoma had 2.5- and 20-fold increased serum sL-selectin
levels, respectively. By contrast, serum sL-selectin levels were
reduced by 70% in Rag-deficient mice lacking mature lymphocytes. The
majority of serum sL-selectin had a molecular mass of 65–75
kDa, consistent with its lymphocyte origin. Slow turnover may explain
the relatively high levels of sL-selectin in vivo. The
t1/2 of sL-selectin, assessed by
transferring sera from wild-type mice into L-selectin-deficient mice
and monitoring serum sL-selectin levels by ELISA, was >20 h, and it
remained detectable for longer than 1 wk. Short-term in vivo lymphocyte
migration assays demonstrated that near physiologic levels (0.9
µg/ml) of sL-selectin decreased lymphocyte migration to peripheral
lymph nodes by >30%, with dose-dependent inhibition occurring with
increasing sL-selectin concentrations. These results suggest that
sL-selectin influences lymphocyte migration in vivo and that the
increased sL-selectin levels present in certain pathologic conditions
may adversely affect leukocyte migration.
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