Immunohistochemical Localization of Intracellular and Extracellular Associated TGFβ in the Skin of Patients with Systemic Sclerosis (Scleroderma) and Primary Raynaud's Phenomenon

Gabrielli, Armando; Loreto, Christina Di; Taborro, R; Candela, Marco; Sambo, Paola; Nitti, C. De; Danieli, M.G.; DeLustro, Frank; Dasch, James R.; Danieli, G

doi:10.1006/clin.1993.1136

Cited by 59 publications

(29 citation statements)

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“…Anti-Fas antibody treatment of TGF␤1-pretreated fibroblasts resulted in proliferation, an effect previously described only in neonatal foreskin fibroblasts (27,33). TGF␤1 is present in nonlesional skin early in the disease, prior to fibrosis (34,35). Thus, TGF␤1 may promote the survival of fibroblasts that are normally targeted to die by infiltrating inflammatory cells in the development of SSc.…”

Section: Discussionmentioning

confidence: 87%

Role of apoptosis and transforming growth factor β1 in fibroblast selection and activation in systemic sclerosis

Jelaska

Korn

2000

Arthritis & Rheumatism

161

110

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Section: Discussionmentioning

confidence: 87%

Role of apoptosis and transforming growth factor β1 in fibroblast selection and activation in systemic sclerosis

Jelaska

Korn

2000

Arthritis & Rheumatism

161

110

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“…Endothelin–1, a potent vasoconstrictor peptide produced by endothelial cells, is elevated in SSc plasma and has been shown to stimulate fibroblast proliferation and collagen synthesis [55, 56]. Immunohistochemistry and in situ hybridization have shown endothelial transforming growth factor beta (TGF–β) expression in SSc skin [57, 58]. TGF–β has been shown to inhibit endothelial cell growth in vitro [59], but to promote angiogenesis in vivo [60].…”

Section: Cytokinesmentioning

confidence: 99%

The Vascular Perspective of Systemic Sclerosis: Of Chickens, Mice and Men

Sgonc

1999

Int Arch Allergy Immunol

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Systemic sclerosis (SSc), or scleroderma, is an autoimmune connective tissue disease characterized by structural and functional vascular abnormalities, perivascular mononuclear cell infiltration, and increased deposition of extracellular matrix in skin and internal organs. The initial stages of SSc are generally not accessible for analysis in man, therefore, the availability of appropriate animal models is of great importance for the elucidation of the pathogenesis of this disease. UCD–200 chickens show the entire clinical, histopathological and serological spectrum of SSc, whereas tight skin (Tsk)1/+ and Tsk2/+ mice, other animal models of scleroderma, lack the vascular injury. A parallel comparative study of skin biopsies of UCD–200 chickens and human SSc patients revealed that endothelial cell apoptosis, induced by anti–endothelial cell antibody (AECA)– dependent cellular cytotoxicity, is a primary event in the pathogenesis of SSc. This review focuses on recently established data on endothelial cell injury in animals with spontaneous disease and humans, AECA, adhesion molecules and cytokine profiles that support a vascular pathogenesis in scleroderma.

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“…IL-4 production by Th2 type T cells induces both the production of transforming growth factor ␤ (TGF␤), a fibroblast mitogen (13)(14)(15), as well as the production of collagen by fibroblasts (16,17). Endothelial cell activation is evident, as suggested by the expression of E-selectin (18)(19)(20), TGF␤ (21), and endothelin 1 (22,23). Monocyte activation is also reported, as documented by increased production in the peripheral blood of superoxide anion (24), , IL-1, and TGF␤ (26).…”

Section: Introductionmentioning

confidence: 99%