Functional renal involvement in normotensive patients with progressive systemic sclerosis. impaired sodium excretion during isotonic saline infusion

Normally, native collagen is resistant to non-specific proteolytic enzymes. Only collagenase can split collagen into two degradation products, TCA and TCB, which can then be degraded by protease. Our studies using human '*C labelled collagen type I as substrate have shown the activity of collagenase to be normal in the serum of progressive systemic sclerosis (PSS) and to be significantly decreased in skin homogenates. In contrast, the azocaseinolytic activity of nonspecific protease (mainly serine protease) was increased approximateiy 7-fold compared to the controls. These findings are surprising, since increased collagen metabolism is generally accepted in PSS. In collagen degradation assays we showed that PSS-serum followed by pronase could degrade collagen, ^-galactosidase followed by cathepsin H, chymotrypsin or trypsin exerted the same effect. Obviously, collagen is deglycosylated by i3-galactosidase,' making it sensitive to proteolytic attack and exhibits different denaturation characteristics. This is also suggested by studies with the Con A affinity gel electrophoresis, as the collagen was no longer retained at the origin after incubation with PSS-serum, and a definite mobility could be shown. Additionaily, galactose and glucose were liberated from collagen type I by /?galactosidase under our degradation conditions. The initial deglycosylation of collagen by jigalactosidase followed by degradation by non-specific protease is interpreted as an aiternative collagen degradation pathway^ in PSS which can compensate for the decreased collagenase activity.

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Early phenotypic activation of circulating helper memory T cells in scleroderma: correlation with disease activity.

Fiocco

Rosada

Cozzi

et al. 1993

Annals of the Rheumatic Diseases

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Objectives-The differential expression of several accessory/activation molecules (CD26, CD29, CD45RA, CD25, MLR4, HLA-DR) on peripheral blood CD4+ and CD8+ T lymphocytes in patients with scleroderma was compared with that in controls and patients with other connective systemic diseases to look for evidence of the involvement of T cells in the disease process of scleroderma. Methods-The two colour expression of surface molecules by circulating T cells was analysed with a panel of monoclonal antibodies and flow cytometry in 17 patients with scleroderma, 10 patients with systemic lupus erythematosus, and five patients with rheumatoid arthritis, and the results compared with those for 10 normal controls. The two colour T CD4+ phenotype was further compared between patients with active and quiescent disease in these patients with scleroderma. The coexpression of surface molecules by CD4+ T cells was also analysed by three colour flow cytometry in eight patients with scleroderma. Results-Patients with scleroderma showed increased CD4+CD26+ and CD4+CD25+ percentages and absolute numbers and decreased CD8+CD29+ percentages compared with controls. Moreover, a significant correlation between the higher CD4+CD26+ T cell percentage and absolute cell numbers with disease activity was observed. Most of the CD4+ peripheral blood T cells from patients with scleroderma showed the CD26+CD45RA-phenotype by three colour flow cytometry analysis. Conclusions-The distinctive pattern of early helper memory T cell activation in these patients with rapidly evolving scleroderma supports the role of a T cell mediated mechanism in the progression of scleroderma.

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Functional renal involvement in normotensive patients with progressive systemic sclerosis. impaired sodium excretion during isotonic saline infusion

Cited by 4 publications

References 17 publications

Factors predicting development of renal involvement in progressive systemic sclerosis

Factors predicting development of renal involvement in progressive systemic sclerosis

Pathogenesis of Progressive Systemic Sclerosis

Early phenotypic activation of circulating helper memory T cells in scleroderma: correlation with disease activity.

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