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Receptor Cross-Linking: Effects on Parenchymal Cell IL-8 Release1
Divisions of
*
Pulmonary and Critical Care Medicine and
Nephrology,
College of Medicine and College of Pharmacy, Ohio State University, Columbus, OH 43210
Neutrophils mediate tissue injury in response to immune complexes,
although the factors that induce their recruitment are incompletely
understood. We have reported that lymphocytes may be important
regulators of monocyte and macrophage IL-8 release in the presence of
immobilized IgG. Since tissue parenchymal cells are important local
producers of IL-8 but are not directly stimulated by Fc
R
cross-linking, we hypothesized that lymphocytes may also regulate
parenchymal IL-8 release. Supernatants from lymphocytes incubated on
immobilized IgG induced primary human fibroblasts and human mesangial
cells to produce IL-8 (17 ± 3.5 and 44 ± 8 ng/ml,
respectively). Fibroblast and mesangial cell IL-8 mRNA levels were
similarly increased by the conditioned lymphocyte supernatant.
Immobilized anti-human FcRIII, but not FcRI or FcRII Abs,
could stimulate this IL-8-inducing activity in lymphocytes, suggesting
that FcRIII-bearing lymphocytes were responsible. Supernatants from
lymphocytes incubated on immobilized IgG contained 2.2 ± 0.8
ng/ml of IL-1ß, while enriched monocyte preparations from the same
donors incubated on immobilized IgG released only 0.1 ± 0.04
ng/ml of IL-1ß (p = 0.05). Consistent with
the identification of IL-1ß as the lymphocyte factor, fibroblast or
mesangial cell IL-8 release induced by the IgG-stimulated lymphocyte
supernatants was inhibited by 1) the combination of IL-1R antagonist
and soluble type II IL-1R, 2) an IL-1-converting enzyme inhibitor, or
3) anti-IL-1ß but not preimmune Abs. These data suggest that
targeted deposits of IgG can stimulate FcRIII-bearing lymphocytes to
produce IL-1ß, which induces parenchymal cell IL-8 release.
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