The aim of our study was to investigate and characterize regulatory T cells (Treg) in peripheral blood of patients with connective tissue diseases (Systemic lupus erythematosus, systemic sclerosis, Sjögren's syndrome, poly- and dermatomyositis) as compared with blood from healthy controls. Treg cells were quantified and phenotypically characterized by flow cytometry while the expression level of Foxp3 mRNA was evaluated by real time PCR. A reduced percentage of peripheral blood Treg cells was found in patients than in controls, irrespective of the type of connective tissue disease. Treg cells, especially those expressing one of the phenotypical markers, seemed to differ not only between patients and healthy controls but also among types of diseases. Additionally, the presence of autoantibodies as well as disease activity appeared to be correlated with particular Treg cell populations, especially those expressing one of the examined phenotypical markers. Correlations with therapy suggested that glucocorticoids plus antimalarial or other immunosuppressor drugs diminished the percentage of Treg cells, especially of those with memory phenotype. These findings indicated dysregulations at the level of Treg cells and suggested an involvement of these cells in the pathology of connective tissue diseases. Moreover, our data are in agreement with the suggestion that Treg cells could be therapeutic targets for some autoimmune diseases.

It was suggested that the immune system plays an important role at least in the amplification of the main elements in systemic sclerosis (SSc), an autoimmune disease with an incompletely elucidated pathogenesis. Elucidation of the mechanisms involved in the interaction between T and B cells, major players of the immune system, could contribute to a better understanding of some of clinical and pathological manifestations of SSc. Recently, abnormalities in Semaphorin 4D (Sema4D/CD100) or CD72, two contrareceptors involved in T and B cells cooperation, were associated with autoimmunity. Therefore, we investigated CD100 and CD72 expression level on T and B cells in attempting to establish their role in SSc pathogenesis. The results revealed augmented percentages of CD100(high) T and B cells, significantly increased expression of CD100 on CD4(+) T cells and frequently detectable levels of soluble CD100 in SSc patient sera compared to healthy donors. In SSc, CD100 dysregulations were associated with anti-Scl70 antibodies production, disease type, thickening of skin, disease duration, or with active inflammation processes. In consequence, dysregulations in CD100 expression and release could play a role in SSc development and/or maintenance.

Our results suggest a new strategy to correct defects in CD4 T cell tolerance mechanisms that may prove beneficial in SLE.

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