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*
Departments of Dermatology and
Pediatrics, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106;
Department of Dermatology, Kyushu University, Fukuoka, Japan; and
§
Veterans Administration Medical Center, Cleveland, OH 44106
CD11b+ monocytic/macrophagic cells (Mo/Mph), which
infiltrate into skin after UV irradiation, play an important role in
UV-induced immunosuppression. Because in mice, blockade of CD11b (iC3b
receptor) on monocytes and depletion of its ligand, iC3b, reverses
UV-induced immunosuppression, we asked whether iC3b is deposited in
human skin after UV, and whether iC3b can modulate the cytokine profile
of Mo/Mph. Immunofluorescence studies revealed that iC3b was newly
deposited in UV-exposed skin and was localized in apposition to
infiltrating CD11b+ Mo/Mph. In addition, in situ
hybridization studies showed that TNF-
mRNA was also induced in a
similar microanatomic localization. To model the effects of these
complex signals on infiltrating Mo/Mph following UV exposure, we then
tested the effects of immobilized iC3b and TNF- on resting blood
monocytes. Both IL-10 mRNA synthesis and protein secretion were
significantly induced by binding of iC3b in vitro and were
synergistically increased by the presence of TNF-. The effect was
abrogated by a blocking Ab to CD11b, indicating CD11b-iC3b interaction.
In contrast, iC3b binding resulted in suppression of IL-12 p40 mRNA and
significantly inhibited the production of IL-12 p70 protein. Our
studies thus define a novel mechanism for induction of tissue Mo/Mph
into an IL-10high/IL-12low state via iC3b in
combination with TNF-.
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