Literature DB >> 30937729

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

Ulana Juhas1, Monika Ryba-Stanisławowska2, Urszula Ławrynowicz2, Małgorzata Myśliwiec3, Jolanta Myśliwska2.   

Abstract

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.

Entities:  

Keywords:  Membrane CD83; Monocyte-derived cells; Soluble CD83; Type 1 diabetes

Mesh:

Substances:

Year:  2019        PMID: 30937729     DOI: 10.1007/s12026-019-09074-y

Source DB:  PubMed          Journal:  Immunol Res        ISSN: 0257-277X            Impact factor:   2.829


  36 in total

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2.  CD83-stimulated monocytes suppress T-cell immune responses through production of prostaglandin E2.

Authors:  Liwen Chen; Yibei Zhu; Guangbo Zhang; Chao Gao; Weixue Zhong; Xueguang Zhang
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3.  The proinflammatory CD14+CD16+DR++ monocytes are a major source of TNF.

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Journal:  J Immunol       Date:  2002-04-01       Impact factor: 5.422

4.  Increased levels of circulating soluble CD14 but not CD83 in infants are associated with early intestinal colonization with Staphylococcus aureus.

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Review 5.  Inflammatory molecules and pathways in the pathogenesis of diabetic nephropathy.

Authors:  Juan F Navarro-González; Carmen Mora-Fernández; Mercedes Muros de Fuentes; Javier García-Pérez
Journal:  Nat Rev Nephrol       Date:  2011-05-03       Impact factor: 28.314

6.  The Analysis of CD83 Expression on Human Immune Cells Identifies a Unique CD83+-Activated T Cell Population.

Authors:  Xinsheng Ju; Pablo A Silveira; Wei-Hsun Hsu; Zehra Elgundi; Renz Alingcastre; Nirupama D Verma; Phillip D Fromm; Jennifer L Hsu; Christian Bryant; Ziduo Li; Fiona Kupresanin; Tsun-Ho Lo; Candice Clarke; Kenneth Lee; Helen McGuire; Barbara Fazekas de St Groth; Stephen R Larsen; John Gibson; Kenneth F Bradstock; Georgina J Clark; Derek N J Hart
Journal:  J Immunol       Date:  2016-11-11       Impact factor: 5.422

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8.  Expansion of CD14+CD16+ monocytes producing TNF-α in complication-free diabetes type 1 juvenile onset patients.

Authors:  Jolanta Myśliwska; Marcin Smardzewski; Natalia Marek-Trzonkowska; Małgorzata Myśliwiec; Krystyna Raczyńska
Journal:  Cytokine       Date:  2012-04-07       Impact factor: 3.861

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Review 2.  The CD83 Molecule - An Important Immune Checkpoint.

Authors:  Linda Grosche; Ilka Knippertz; Christina König; Dmytro Royzman; Andreas B Wild; Elisabeth Zinser; Heinrich Sticht; Yves A Muller; Alexander Steinkasserer; Matthias Lechmann
Journal:  Front Immunol       Date:  2020-04-17       Impact factor: 7.561

  2 in total

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