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Article
September 1, 1989

On SclerodermaMast Cells, Endothelial Cells, and Fibroblasts

Author Affiliations

From the Departments of Medicine and Microbiology/Immunology, University of Colorado School of Medicine, Denver.

From the Departments of Medicine and Microbiology/Immunology, University of Colorado School of Medicine, Denver.

JAMA. 1989;262(9):1206-1209. doi:10.1001/jama.1989.03430090068035
Abstract

An integrated view of the pathogenesis of scleroderma should include vascular, immunologic, and fibrotic processes. This review introduces the mast cell into this picture, emphasizing recent knowledge gained from a study of experimental chronic graft-vs-host disease and scleroderma itself. In both of these situations, increased mast cell activity occurs. A link between the activation of both endothelial cells and fibroblasts may be provided by the family of heparin-binding growth factors. These cytokines are produced by many cells and are bound, protected, and enhanced by heparin, which may be provided by the activated mast cells. These and other growth factors may be responsible for endothelial proliferation and excess collagen production by fibroblasts. This enlarged schema should provide additional points for therapeutic intervention in scleroderma.

(JAMA. 1989;262:1206-1209)

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