SSCS, EUSTAR, EUVAS, auto-immunité, inflammation, fibrose.
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English summary: inflammation and fibrosis
The pathogenic mechanisms leading to fibrosis are still incompletely understood and the available therapeutic approaches of limited efficacy. To test the hypothesis that T cells and antifibroblast autoantibodies (AFA) may be directly involved in the dysregulation of extracellular matrix (ECM) deposition by fibroblasts, and that fibroblasts may contribute to inflammatory responses, we have set up an in vitro model where fibroblasts are submitted to the influence of T cells or AFA.
We have taken as disease model systemic sclerosis (SSc), a condition of possible auto-immune origin, characterized by widespread fibrosis involving the skin and internal organs and fibroproliferative microangiopathy. We have recently found that proteasome blockade profoundly modifies fibroblast metabolism favoring collagenolyic activity over collagen deposition, therefore resulting in an anti-fibrotic phenotype. We are exploring the role of the unfolded protein response (UPR) in ECM regulation. We are extending our observations to in vivo models of fibrosis.
From the clinical point of view, we participate to international coordinated efforts for improving the knowledge on systemic sclerosis as active members of EUSTAR (Eular scleroderma trial and research). We are founders and active members of SSCS (Swiss Systemic Lupus Erythematosus Cohort Study) aimed at improving the knowledge on systemic lupus erythematosus.