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Research Article Free access | 10.1172/JCI115385
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
Find articles by Zhang, Y. in: JCI | PubMed | Google Scholar
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
Find articles by Ramos, B. in: JCI | PubMed | Google Scholar
Department of Pharmacology, Washington University School of Medicine, St. Louis, Missouri 63110.
Find articles by Jakschik, B. in: JCI | PubMed | Google Scholar
Published September 1, 1991 - More info
Immune complex-induced injury is an important pathogenic factor in antibody-mediated nephritis, systemic lupus erythematosus, rheumatoid arthritis, and other diseases. In this study we investigated the role mast cells in immune complex-mediated injury in mouse skin. Reverse Arthus reaction was induced in mast cell-deficient WBB6F1-W/Wv mice and their congenic controls (WBB6F1(-)+/+). Serial skin sections were evaluated for neutrophil infiltration, edema, and hemorrhage. In WBB6F1-W/Wv mice the neutrophil influx was only 40% and edema 60% of that in congenic controls. Hemorrhage was also significantly reduced in the mast cell-deficient mice. After mast cell reconstitution, the magnitude of the reaction in WBB6F1-W/Wv was equivalent to that in WBB6F1(-)+/+ mice. Mast cell release in reverse Arthus reaction was evaluated by measuring fluorescence intensity after avidin-FITC staining of mast cell granules. There was a 70% decrease in fluorescence intensity. The 5-lipoxygenase inhibitor A-63162 significantly decreased neutrophil accumulation (40%), edema (60%), and hemorrhage in WBB6F1(-)+/+, but not in mast cell-deficient mice. Mast cell reconstitution of WBB6F1-W/Wv mice restored the effect of A-63162. The results indicate that mast cells and their mediators, including leukotrienes, make an important contribution to reverse Arthus reaction.
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