Lymphocytes Produce IL-1β in Response to Fcγ Receptor Cross-Linking: Effects on Parenchymal Cell IL-8 Release

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