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DOI 10.1007/s12026-019-09074-y

Медицинская библиотека · Immunologic research · 2019

Putative loss of CD83 immunosuppressive activity in long-standing complication-free juvenile diabetic patients during disease progression.

Juhas Ulana, Ryba-Stanisławowska Monika, Ławrynowicz Urszula, Myśliwiec Małgorzata, Myśliwska Jolanta

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

The CD83 molecule is a known marker of dendritic cell differentiation process, and its soluble form (sCD83) exerts immunosuppressive functions. In our research, we examined whether the sCD83 plasma concentration is impaired in DM1 children and if the expected changes are in line with the disturbed process of monocyte's transformation into mCD83+ monocyte-derived cells. 28 newly diagnosed (ND-DM1) and 30 long-standing (LS-DM1) patients were enrolled into our study. We revealed that the examined cells show a high mCD83 expression level in ND-DM1, which was significantly downregulated by the TNF-α stimulation. The results were in line with those from healthy controls. We also observed that monocyte differentiation process into CD83+ cells was much defective in LS-DM1 children and the mCD83 expression level seems not to be controlled by TNF-α. Moreover, the sCD83 level was significantly decreased in plasma from LS-DM1 children and it was negatively related to HbA1c levels, while no correlations were observed between TNF-α plasma concentration or disease duration. Summarizing, our results suggest that reduced sCD83 levels may correspond with a poor metabolic control in LS-DM1 patients and therapeutic administration of this molecule may indicate a new therapy approach in the chronic phase of diabetes.

Для цитирования: Juhas Ulana, Ryba-Stanisławowska Monika, Ławrynowicz Urszula, Myśliwiec Małgorzata, Myśliwska Jolanta. Putative loss of CD83 immunosuppressive activity in long-standing complication-free juvenile diabetic patients during disease progression.. Immunologic research. 2019. DOI: 10.1007/s12026-019-09074-y.

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