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23. Gelatinase B–deficient Mice Are Resistant to Experimental Bullous Pemphigoid

Author

Liu, Zhi, Shipley, J Michael, Vu, Thiennu H, Zhou, Xiaoye, Diaz, Luis A, Werb, Zena, and Senior, Robert M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Autoimmune Disease, 2.1 Biological and endogenous factors, Aetiology, Animals, Antibodies, Autoantigens, Collagenases, Disease Models, Animal, Gene Deletion, Humans, Immunity, Innate, Matrix Metalloproteinase 9, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Neutrophils, Non-Fibrillar Collagens, Pemphigoid, Bullous, Rabbits, autoimmunity, basement membrane zone, hemidesmosome, inflammation, mouse model, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease characterized by deposition of autoantibodies at the basement membrane zone. In an experimental BP model in mice, the subepidermal blistering is mediated by antibodies directed against the hemidesmosomal protein BP180 (collagen XVII, BPAG2), and depends on complement activation and neutrophil infiltration. Gelatinase B is present in BP blister fluid and can cleave BP180. In this study we investigated the role of gelatinase B in the immunopathogenesis of experimental BP using mice containing targeted disruption of the gelatinase B (MMP-9, 92 kD gelatinase) gene. Gelatinase B-deficient mice were resistant to the blistering effect of intracutaneous anti-mBP180 antibodies, although these mice showed deposition of autoantibodies at the basement membrane zone and neutrophil recruitment to the skin comparable to that observed in the control mice. Interleukin 8 given intradermally concomitantly with pathogenic anti-mBP180 elicited a significant neutrophil recruitment into the skin in gelatinase B-deficient mice, but blistering did not occur. However, gelatinase B-deficient mice reconstituted with neutrophils from normal mice developed blistering in response to anti-mBP180 antibodies. These results implicate neutrophil-derived gelatinase B in the pathogenesis of experimental BP and might lead to novel therapeutic strategies for BP.

Published
1998

40. The serpin alpha1-proteinase inhibitor is a critical substrate for gelatinase B/MMP-9 in vivo

Author

Liu, Zhi, Zhou, Xiaoye, Shapiro, Steven D., Shipley, J. Michael, Twining, Sally S., Diaz, Luis A., Senior, Robert M., and Werb, Zena

Subjects
Blisters -- Physiological aspects, Bullous pemphigoid -- Physiological aspects, Protein research -- Analysis, Enzyme inhibitors -- Physiological aspects, Biological sciences
Abstract

Research demonstrates the functional interactions between gelatinase B/MMP-9 and neutrophil elastase in the blister formation in bullous pemphigoid disease condition. Data indicate that serpin alpha1-proteinase inhibitor acts as a substrate of the former enzyme, which is cleaved in vivo during dermal-epidermal separation leading to blisters.

Published
2000

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