Literature DB >> 19499249

The prevalence of Th17 cells and FOXP3 regulate T cells (Treg) in children with primary nephrotic syndrome.

Xiao Shan Shao1, Xi Qang Yang, Xiao Dong Zhao, Qiu Li, Yuan Yuan Xie, Xiao Gang Wang, Mo Wang, Wei Zhang.   

Abstract

The aim of this study was to investigate the prevalence of interleukin (IL)-17-producing CD4+ T cells (Th17) and regulatory T (Treg) cells in children with primary nephrotic syndrome. The study cohort consisted of 62 children who were randomly divided into control, primary nephrotic syndrome, and isolated hematuria groups. Flow cytometric analysis revealed the presence of Th17 cells in the peripheral blood mononuclear cells (PBMCs) of 35 children and Tregs in the PBMCs of all children. In addition, mRNA expression of Th17-related factors [IL-17, -23p19 and retinoid orphan nuclear receptor (RORc)] and the concentration of plasma inflammatory mediators such as IL-6 and IL-1beta were consistently detected in all children. Protein expression of IL-17 and transforming growth factor-beta1 were also detected in renal biopsy tissue and compared between different groups. Patients with PNS were found to have an increased number of Th17 cells and decreased numbers of Tregs in their PBMCs, and there was significant difference in the prevalence of Th17 and Tregs between the patients with PNS and those with isolated hematuria. Our data show that among our study cohort, there was a dynamic equilibrium between Th17 and Treg cells in children with PNS following the development of PNS with apparent renal tubular epithelial cell and interstitium lesions. The dynamic interaction between Th17 and Treg cells may be important in the development of PNS.

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Year:  2009        PMID: 19499249     DOI: 10.1007/s00467-009-1194-x

Source DB:  PubMed          Journal:  Pediatr Nephrol        ISSN: 0931-041X            Impact factor:   3.714


  26 in total

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Journal:  Nature       Date:  2006-04-30       Impact factor: 49.962

2.  Pathogenesis of lipoid nephrosis: a disorder of T-cell function.

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4.  Overload proteinuria is followed by salt-sensitive hypertension caused by renal infiltration of immune cells.

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  34 in total

Review 1.  The role of the immune system in idiopathic nephrotic syndrome: a review of clinical and experimental studies.

Authors:  Wagner de Fátima Pereira; Gustavo Eustáquio Alvim Brito-Melo; Fábio Tadeu Lourenço Guimarães; Thiago Guimarães Rosa Carvalho; Elvis Cueva Mateo; Ana Cristina Simões e Silva
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Review 2.  Immunology of idiopathic nephrotic syndrome.

Authors:  Manuela Colucci; Giorgia Corpetti; Francesco Emma; Marina Vivarelli
Journal:  Pediatr Nephrol       Date:  2017-04-27       Impact factor: 3.714

3.  Characterisation of renal immune cell infiltrates in children with nephrotic syndrome.

Authors:  Kerstin Benz; Maike Büttner; Katalin Dittrich; Valentina Campean; Jörg Dötsch; Kerstin Amann
Journal:  Pediatr Nephrol       Date:  2010-04-13       Impact factor: 3.714

Review 4.  Physiopathology of idiopathic nephrotic syndrome: lessons from glucocorticoids and epigenetic perspectives.

Authors:  Valéry Elie; May Fakhoury; Georges Deschênes; Evelyne Jacqz-Aigrain
Journal:  Pediatr Nephrol       Date:  2011-06-28       Impact factor: 3.714

5.  Toll-like receptor 3 expression and function in childhood idiopathic nephrotic syndrome.

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6.  Interleukin-1 accounts for intrarenal Th17 cell activation during ureteral obstruction.

Authors:  Jana Pindjakova; Shirley A Hanley; Michelle M Duffy; Caroline E Sutton; Gudrun A Weidhofer; Melinda N Miller; Karl A Nath; Kingston H G Mills; Rhodri Ceredig; Matthew D Griffin
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7.  Inactivation of Notch signaling reverses the Th17/Treg imbalance in cells from patients with immune thrombocytopenia.

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8.  MicroRNA-155 deficiency promotes nephrin acetylation and attenuates renal damage in hyperglycemia-induced nephropathy.

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Review 9.  Rituximab therapy in nephrotic syndrome: implications for patients' management.

Authors:  Aditi Sinha; Arvind Bagga
Journal:  Nat Rev Nephrol       Date:  2013-01-22       Impact factor: 28.314

10.  Myocardial infarction worsens glomerular injury and microalbuminuria in rats with pre-existing renal impairment accompanied by the activation of ER stress and inflammation.

Authors:  Zhifeng Dong; Penglong Wu; Yongguang Li; Yuan Shen; Ping Xin; Shuai Li; Zhihua Wang; Xiaoyan Dai; Wei Zhu; Meng Wei
Journal:  Mol Biol Rep       Date:  2014-08-31       Impact factor: 2.316

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