cutaneous chronic graft-versus-host disease does not have the abnormal endothelial phenotype or vascular rarefaction characteristic of systemic sclerosis皮肤慢性移植物抗宿主病没有异常的内皮细胞表型或血管稀疏系统性硬化病的特征.pdfVIP

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cutaneous chronic graft-versus-host disease does not have the abnormal endothelial phenotype or vascular rarefaction characteristic of systemic sclerosis皮肤慢性移植物抗宿主病没有异常的内皮细胞表型或血管稀疏系统性硬化病的特征.pdf

cutaneous chronic graft-versus-host disease does not have the abnormal endothelial phenotype or vascular rarefaction characteristic of systemic sclerosis皮肤慢性移植物抗宿主病没有异常的内皮细胞表型或血管稀疏系统性硬化病的特征

Cutaneous Chronic Graft-Versus-Host Disease Does Not Have the Abnormal Endothelial Phenotype or Vascular Rarefaction Characteristic of Systemic Sclerosis 1 1,2 3 3 3 Jo Nadine Fleming *, Howard M. Shulman , Richard A. Nash , Pamela Y. Johnson , Thomas N. Wight , Allen Gown4, Stephen M. Schwartz1 1 Department of Pathology, University of Washington, Seattle, Washington, United States of America, 2 Clinical Research Division, Pathology Section, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America, 3 Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America, 4 Benaroya Research, Seattle, Washington, United States of America, 5 Phenopath Laboratories, Seattle, Washington, United States of America Abstract Background: The clinical and histologic appearance of fibrosis in cutaneous lesions in chronic graft-versus -host disease (c- GVHD) resembles the appearance of fibrosis in scleroderma (SSc). Recent studies identified distinctive structural changes in the superficial dermal microvasculature and matrix of SSc skin. We compared the dermal microvasculature in human c- GVHD to SSc to determine if c-GVHD is a suitable model for SSc. Methodology/Principal Findings: We analyzed skin biopsies of normal controls (n = 24), patients with SSc (n = 30) and c- GVHD with dermal fibrosis (n = 133)). Immunostaining was employed to identify vessels, vascular smooth muscle, dermal matrix, and cell proliferation. C-GVHD and SSc had similar dermal matrix composition and vascular smooth muscle pathology, including intimal hyperplasia. SSc, however, differed significantly from c-GVHD in three ways. First, there were

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