Differential alteration in peripheral T-regulatory and T-effector cells with change in P-glycoprotein expression in Childhood Nephrotic Syndrome: A longitudinal study

Prasad, Narayan; Jaiswal, Akhilesh; Agarwal, Vikas; Chae, Soryong; Sharma, Raj Kumar; Rai, Mohit; Singh, Harshinder; Chaturvedi, Saurabh; Singh, Ajay K.

doi:10.1016/j.cyto.2014.12.028

Cited by 45 publications

(39 citation statements)

References 34 publications

(30 reference statements)

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“…Since then, Treg have drawn particular attention as key players in the pathogenesis of INS. Treg involvement has been suggested not only in clinical studies, but also in experimental models: Le Berre et al . showed that the transfer of Treg to Buff/Mna rats, which spontaneously develop nephrotic syndrome, significantly reduced proteinuria.…”

Section: Discussionmentioning

confidence: 99%

“…Conventionally, the etiology of idiopathic nephrotic syndrome (INS), in which minimal change nephrotic syndrome (MCNS) accounts for the vast majority of histology, has been attributed to impaired T cells. 1,2 Since the first description of a boy with immune dysregulation, polyendocrinopathy, enteropathy, Xlinked (IPEX) syndrome characterized by a paucity of regulatory T cells (Treg) complicated by MCNS, 3 Treg have drawn special attention as a key player in the pathogenesis of INS: several studies have shown that Treg are reduced in number in patients with active INS or MCNS, [4][5][6] although there are some contradictory results. 7 Regulatory T cells were originally identified as CD4positive, CD25-positive, Forkhead box P3 (Foxp3)-positive T cells regulating inhibitory control of immune responses.…”

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confidence: 99%

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Regulatory T cells and CTLA‐4 in idiopathic nephrotic syndrome

Tsuji

Kimata

Yamanouchi

et al. 2017

Pediatrics International

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The pathogenesis of idiopathic nephrotic syndrome (INS) remains unknown. Recently, it was postulated that suppression of regulatory T cells (Treg) leads to massive proteinuria in INS, although there is some controversy. Considering the important role of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) in Treg-mediated immune suppression, the aim of this study was therefore to clarify the involvement of Treg and CTLA-4 in the pathogenesis of INS. Fifteen patients with INS were enrolled. Their blood was sampled twice, once at onset and once at remission induced by glucocorticoid. Although median Treg number was significantly lower at onset than in healthy children, it increased at remission. Similarly, serum CTLA-4 concentration significantly increased at remission compared with onset. Furthermore, a positive significant correlation was observed between Treg number and serum CTLA-4 level. This suggests that Treg and CTLA-4 are involved in the induction of remission in INS.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Regulatory T cells and CTLA‐4 in idiopathic nephrotic syndrome

Tsuji

Kimata

Yamanouchi

et al. 2017

Pediatrics International

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“…inducing a transient or persistent massive proteinuria, typically triggered by viral or bacterial infections, allergen-or T-cell-mediated release of cytokines (e.g., interleukin-13). 10,11 An association between various cytokines, circulatory factors and proteinuria have been shown to affect glomerular permeability, 12 importantly, an increase in monocyte/macrophage cytokines, including interleukin IL1, IL12, IFN- and TNF-α, were shown to be responsible for initiation and recurrence of INS. 13 IFN- is secreted from T-helper cells, cytotoxic T cells, natural killer cells, and macrophages.…”

Section: Interferon Gamma (Ifn-) a Pro-inflammatory Cytokine Is Thmentioning

confidence: 99%

Interferon gamma: is it a co-player in the pathogenesis of idiopathic nephrotic syndrome?

Hassan

El-Hakim

Amr

et al. 2020

Egypt J Pediatr Allergy Immunol

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“…Patients with INS respond favorably to steroids; however, a number of patients with INS may suffer from frequent relapses or develop dependence on or resistance to steroids in the later stage, leading to a protracted course (1,2). Although exact pathogenic mechanisms of INS remain unclear, altered immunological responses, cellular oxidative stress, and genetic aberration have been proposed (3). Inflammatory cascades involving production of free radicals and their role in alteration of glomerular hemodynamics have also been suggested to have a role in pathogenesis of nephrotic syndrome (NS).…”

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confidence: 99%

NOX-mediated impairment of PDGF-induced DNA synthesis in peripheral blood lymphocytes of children with idiopathic nephrotic syndrome

Al‐Eisa

Dhaunsi

2017

Pediatr Res

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BackgroundCellular oxidative stress, inflammatory responses, and immunogenic events are involved in pathogenesis of idiopathic nephrotic syndrome (INS); however, the exact mechanism remains unknown. We examined NADPH oxidase (NOX) activity and platelet-derived growth factor (PDGF)-induced DNA synthesis in peripheral blood lymphocytes (PBL) of patients with INS.MethodsPBL from 15 patients with INS and 15 age- and gender-matched controls were isolated, and enzyme activities of NOX, catalase, and superoxide dismutase (SOD) were measured along with the assay of malondialdehyde levels and bromo-deoxyuridine incorporation. Protein expression of NOX-1 was measured using western blot analysis.ResultsPatients with INS had significantly (P<0.01) higher NOX activity and increased protein expression of NOX-1 in PBL as compared with controls. Catalase and SOD activities were markedly lower with lipid peroxide levels significantly (P<0.01) increased in patients with INS. Ex vivo DNA synthesis in PDGF-stimulated PBL was significantly (P<0.01) reduced in patients with INS; however, diphenyliodonium, an inhibitor of NOX, markedly corrected impairment in growth factor-induced BrdU incorporation.ConclusionsThese results show that NOX activation might have a role in regulation of lymphocytic activity in patients with INS through the impairment of PDGF mitogenic function and might contribute toward pathogenesis of nephrotic syndrome.

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Differential alteration in peripheral T-regulatory and T-effector cells with change in P-glycoprotein expression in Childhood Nephrotic Syndrome: A longitudinal study

Cited by 45 publications

References 34 publications

Regulatory T cells and CTLA‐4 in idiopathic nephrotic syndrome

Regulatory T cells and CTLA‐4 in idiopathic nephrotic syndrome

Interferon gamma: is it a co-player in the pathogenesis of idiopathic nephrotic syndrome?

NOX-mediated impairment of PDGF-induced DNA synthesis in peripheral blood lymphocytes of children with idiopathic nephrotic syndrome

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