Imbalance of Th1/Th2 transcription factors in patients with lupus nephritis

Chan, Rebecca Wing-Yan; Lai, Fernand M.M.; Li, E. K.-M.; Tam, Lai‐Shan; Chow, Kai‐Ming; Li, P. K.-T.; Szeto, Cheuk‐Chun

doi:10.1093/rheumatology/kel029

Cited by 86 publications

(78 citation statements)

References 32 publications

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“…In another study, expression of miR-146a was shown to be involved in level of inflammation and thus can determine histological activity index (25). It has been also identified a functional variant in the promoter of miR-146a associated with LN risk (26,27). We could not show any significant role for miR-198 in pathogenesis of LN.…”

Section: Discussioncontrasting

confidence: 54%

Assessment of microRNA profile of kidney biopsies of patients with lupus nephritis

Malakoutian¹,

Hajian²,

Ebrahimi³

et al. 2017

J Nephropathol

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Background: The changes in some epigenetic elements such as microRNAs result in aberrant immune responses leading to production and secretion of nephritogenic autoantibodies as the main fundament of lupus nephritis (LN).Objectives: The present study aimed to assess the miRNA profile of kidney biopsies in patients with LN with the purpose of describing the critical role of these elements in LN creation. Patients and Methods:In this case-control single center study 11 patients who suffered LN (as the case group) and 11 patients with normal kidney function who were candidate for nephrectomy due to cancer or cyst (as the control group) were included. Kidney biopsies were taken from all LN and control subjects. RNA was extracted and converted to cDNA, then the cDNA was evaluated using NANODROP and then intra-renal expression of candidate miRNAs were quantified in the two groups. In the present study, four topranked miRNAs, miR-638, miR-146a, miR-198, and miR-731 were selected for qRT-PCR. Results: Consistent with the microarray data, we found no significant difference in the expression of all miRNAs between LN and control groups. Using REST 2009 software, we did not also reveal any difference in expression of four miRNAs studied between the patients with LN and those without LN in both parametric and nonparametric patterns. Conclusions:The expression of miR-638, miR-146a, miR-198, and miR-731 may not be related to occurrence of LN in Iranian population.

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Section: Discussioncontrasting

confidence: 54%

Assessment of microRNA profile of kidney biopsies of patients with lupus nephritis

Malakoutian¹,

Hajian²,

Ebrahimi³

et al. 2017

J Nephropathol

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“…Furthermore, patients with SLE show elevated levels of T-bet mRNA and T-bet protein in the urinary sediment and kidney tissues (Chan et al, 2006b;Chan et al, 2006a).…”

Section: T-bet Seems To Have a Pathogenic Role In Systemic Lupus Erytmentioning

confidence: 99%

Role of IFN-α/β signaling in the prevention of genital herpes virus type 2 infection

Svensson

Bellner

Magnusson

et al. 2007

Journal of Reproductive Immunology

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Genital herpes, caused by herpes simplex virus type 2 (HSV-2), is the most common genital ulcer disease worldwide. HSV-2 infection causes a variety of symptoms, ranging from subclinical/silent infection to severe and recurrent episodes of genital blisters and ulcers, and the virus can also in rare cases cause meningitis. In primary infection, the virus sequentially enters and replicates in epithelial cells followed by local sensory neurons. In the latter, a life-long infection is established via the induction of viral latency or dormancy. Latent virus is however continuously reactivated, also in those with a silent infection, which results in a low-grade viral replication and shedding into the vaginal lumen. This reactivation can in many individuals be amplified following e.g. stress, hormonal variations or immune suppression, which results in recurrent genital disease.

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“…Immunological alterations of SLE include apoptotic cell clearance deficiency, complement activation and autoantibody production. An imbalance in T helper type 1 (Th1)/Th2 response has been regarded as a major factor in SLE pathogenesis, with some studies reporting skewing towards Th2 response in peripheral blood mononuclear cells (PBMC), whereas immunopathology studies have shown a predominant Th1 response in proliferative lupus nephritis (LN) [2,3]. Recently, other T cell subsets such as Th17 and regulatory T cells (T reg cells) have been implicated in the SLE immunological scenario [4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

CD4+ T helper cells and regulatory T cells in active lupus nephritis: an imbalance towards a predominant Th1 response?

Mesquita

Kirsztajn

Franco

et al. 2017

Clinical and Experimental Immunology

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SummaryThe objective of this study was to evaluate the frequency of CD4 1 T cell subsets in peripheral blood mononuclear cells (PBMC), urine and renal tissue from patients with lupus nephritis (LN). PBMC and urinary cells were collected from 17 patients with active LN, 20 disease controls (DC) with primary glomerulonephritis and 10 healthy controls (HC) and were analysed by flow cytometry with markers for T helper type 1 (Th1), Th2, Th17 and regulatory T cells (T reg ) cells. T cell subsets were assessed by immunohistochemistry from LN biopsy specimens from 12 LN patients. T cell subtypes in PBMC were re-evaluated at 6 months of therapy. CD4 1 T cells were decreased in PBMC in LN compared with DC and HC (P 5 0Á0001). No differences were observed in urinary CD4 1 T cell subsets between LN and DC. The frequency of urinary Th17 cells was higher in patients with non-proliferative than in proliferative LN (P 5 0Á041). CD3 1 and T-box 21 (T 1 bet ) cells were found in glomeruli and interstitium of LN patients, while forkhead box protein 3 (FoxP3), retinoid-related orphan receptor gamma (ROR-g) and GATA binding protein 3 (GATA-3) were present only in glomeruli. Th1 cells in PBMC were correlated negatively with urinary Th1 cells (Rho 5 -0Á531; P 5 0Á028) and with T bet in renal interstitium (Rho 5 -0Á782; P 5 0Á004). At 6 months, LN patients showed an increase in Th17 cells in PBMC. In conclusion, the inverse association between Th1 cells from PBMC and urinary/renal tissue indicate a role for Th1 in LN pathophysiology. Urinary Th17 cells were associated with less severe LN, and Th17 increased in PBMC during therapy. Urinary CD4 1 T cells were not different between LN and DC.

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Imbalance of Th1/Th2 transcription factors in patients with lupus nephritis

Abstract: Patients with active lupus nephritis have increased T-bet and depressed GATA-3 expression in the urinary sediment and kidney tissue, indicating a predominant Th1 type of T-lymphocyte activation.

Cited by 86 publications

References 32 publications

Assessment of microRNA profile of kidney biopsies of patients with lupus nephritis

Assessment of microRNA profile of kidney biopsies of patients with lupus nephritis

Role of IFN-α/β signaling in the prevention of genital herpes virus type 2 infection

CD4+ T helper cells and regulatory T cells in active lupus nephritis: an imbalance towards a predominant Th1 response?

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