Lidia Rudnicka's early work was related to the role of Natural Killer Cells and adhesion molecules in systemic sclerosis (scleroderma) and showed that activated peripheral blood mononuclear cells of scleroderma patients exhibit increased adhesion to vascular endothelial cells, which is an early event, preceding formation of perivascular lymphocytic infiltrates and development of skin fibrosis.
She is the author of the hypothesis linking etiology of systemic sclerosis to a mutation in the topoisomerase I gene and abnormal topoisomerase I expression. Furthermore, professor Rudnicka believes that presence of anti-topoisomerse I antibodies in sera of patients with scleroderma represents a protective reaction to these abnormalities.
This hypothesis was partly confirmed by Lidia Rudnicka's and her students' studies. The study on which Urszula Nowicka's doctoral thesis was based showed a mutation in the 3’ coding region of the topoisomerase gene in 56% of patients with anti-topo I – positive (Scl70-positive) systemic sclerosis. It was also indicated that specific antibodies penetrate into the nuclei of fibrobasts and inhibit the activity of topoisomerase I. Moreover, the studies evidenced that topoisomerase I inhibitor, campothecin, down-regulates the expression of type I collagen in fibroblasts of scleroderma patients and yields immunosuppressive effects. Certain cytokines were shown to increase the activity of topoisomerase I in dermal.
The hypothesis by professor Rudnicka was discussed during medical conferences, but was never confirmed by other researchers. However, the findings related to the role of campothecin and its potential therapeutical use were reaffirmed in the study by Zhang et al. conducted in patients with keloid.
Another observation by Lidia Rudnicka and her co-workers, which may be potentially beneficial as far as managing systemic sclerosis is concerned, was abnormally high expression of prolactin in peripheral mononuclear cells obtained from patients
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