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*
Department of Dermatology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan; and
Department of Immunology, Duke University Medical Center, Durham, NC 27710
The deposition of immune complexes (IC) induces an acute
inflammatory response with tissue injury. IC-induced inflammation is
mediated by inflammatory cell infiltration, a process highly regulated
by expression of multiple adhesion molecules. To assess the role of
L-selectin and ICAM-1 in this pathogenetic process, the cutaneous
reverse passive Arthus reaction was examined in mice lacking L-selectin
(L-selectin-/-), ICAM-1 (ICAM-1-/-), or
both (L-selectin/ICAM-1-/-). Edema and hemorrhage, which
peaked 4 and 8 h after IC challenge, respectively, were
significantly reduced in L-selectin-/-,
ICAM-1-/-, and L-selectin/ICAM-1-/- mice
compared with wild-type littermates. In general, edema and hemorrhage
were more significantly inhibited in ICAM-1-/- mice than
in L-selectin-/- mice, but were most significantly
reduced in L-selectin/ICAM-1-/- mice compared with
ICAM-1-/- or L-selectin-/- mice. Decreased
edema and hemorrhage correlated with reduced neutrophil and mast cell
infiltration in all adhesion molecule-deficient mice, but leukocyte
infiltration was most affected in L-selectin/ICAM-1-/-
mice. Reduced neutrophil and mast cell infiltration was also observed
for all mutant mice in the peritoneal Arthus reaction. Furthermore,
cutaneous TNF-
production was inhibited in each deficient mouse,
which paralleled the reductions in cutaneous inflammation. These
results indicate that ICAM-1 and L-selectin cooperatively contribute to
the cutaneous Arthus reaction by regulating neutrophil and mast cell
recruitment and suggest that ICAM-1 and L-selectin are therapeutic
targets for human IC-mediated disease.
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