期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 169, 期 3, 页码 954-966出版社
ELSEVIER SCIENCE INC
DOI: 10.2353/ajpath.2006.060205
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资金
- NATIONAL CANCER INSTITUTE [R01CA105001, R01CA096547] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI056363] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA105001, CA96547, R01 CA096547, CA105001] Funding Source: Medline
- NIAID NIH HHS [AI56363, U19 AI056363] Funding Source: Medline
Systemic sclerosis (scleroderma) is an autoimmme disease characterized by excessive extracellular matrix deposition in the skin. A direct role for B lymphocytes in disease development or progression has remained controversial, although autoantibody production is a feature of this disease. To address this issue, skin sclerosis and autoimmunity were assessed in tight-skin mice, a genetic model of human systemic sclerosis, after circulating and tissue B-cell depletion using an anti-mouse CD20 monoclonal antibody before (day 3 after birth) and after disease development (day 56). CD20 monoclonal antibody treatment (10 to 20 fig) depleted the majority (85 to 99%) of circulatig and tissue B cells in newborn and adult tight-skin mice by days 56 and 112, respectively. B-cell depletion in newborn tight-skin mice significantly suppressed (similar to 43%) the development of skin fibrosis, autoantibody production, and hypergammaglobulinemia. B-cell depletion also restored a more normal balance between Th1 and Th2 cytokine mRNA expression in the skin. By contrast, B-cell depletion did not affect skin fibrosis, hypergammaglobulinemia, and autoantibody levels in adult mice with established disease. Thereby, B-cell depletion during disease onset suppressed skin fibrosis, indicating that B cells contribute to the initiation of systemic sclerosis pathogenesis in tight-skin mice but are not required for disease maintenance.
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