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Fibrosis is a pathological manifestation in which connective tissue replaces normal one. It can affect many tissues from the skin to internal organs such as the lungs. Manifestations of pulmonary involvement can be pulmonary arterial hypertension or pulmonary fibrosis. The latter one is currently the leading cause of death in various autoimmune diseases, including systemic sclerosis. Our study group consists of 50 patients with systemic sclerosis: 24 with limited cutaneous form and 26 with diffuse cutaneous form. This cohort was compared to 50 healthy controls (age and sex matched); our aim is to explore the distribution of TH17 cells (TH17) as well as regulatory T cells (TREG) and study their correlation with the disease's progress. Our results show an increase for IL17A in patients compared to controls and that this increase is correlated with a specific clinical involvement: Pulmonary fibrosis. This correlation suggests a crucial role of IL17A in fibrosis especially in systemic sclerosis. In addition, we have shown that the percentages of TH17 cells are higher in patients; however, the percentages of TREG cells are similar between patients and controls. A study of TREG cell activity showed that TREG lost suppressive activity by inactivating the FOXP3 transcription factor. This proves that despite their presence, TREG does not adequately carry out their regulatory activity. Finally, we analyzed the correlation between TH17/TREG and clinical damage; the results show a positive correlation with pulmonary involvement proving the role of TH17/TREG balance in induced fibrosis in systemic sclerosis. No significative difference was observed, for all the parameters, between the two different forms of the disease. In conclusion, the results associated with the TH17/TREG scale and their correlations with fibrosis in systemic sclerosis open a way for new tools to manage this autoimmune disease, which up to today has neither treatment nor accurate diagnosis., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Masson SAS. All rights reserved.)