Donor or recipient TNF-A −308G/A polymorphism and acute rejection of renal allograft: A meta-analysis

Hu, Xin; Bai, Yi; Li, Siyue; Zeng, Ke; Xu, Luhang; Liu, Zhenhua; Song, Xingbo; Lu, Xiaojun; Wang, Lanlan; Ying, Binwu

doi:10.1016/j.trim.2011.04.004

Cited by 22 publications

(12 citation statements)

References 57 publications

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“…Many studies have investigated the association between cytokine gene polymorphisms and acute renal graft rejection, with different studies reporting different results. [1,3,5,17–25] The variable clinical diagnostic processes, different PRA, HLA match status, immunosuppressive protocols, small sample size, and ethnicity may be the main reasons for the inconsistent results of different studies [26,27]. …”

Section: Discussionmentioning

confidence: 99%

Association Between Cytokines and Their Receptor Antagonist Gene Polymorphisms and Clinical Risk Factors and Acute Rejection Following Renal Transplantation

Xie

Wan

2016

Med Sci Monit

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BackgroundAcute rejection (AR) after renal transplantation affects both patient and graft survival. There is growing evidence of the genetic association between cytokine or its receptor antagonist and AR in solid organ transplantation. The objectives of this study were to investigate the role of recipient TNF β, IL-10, IL-1β, and IL-1 receptor antagonist (ra) gene polymorphism, as well as traditional clinical variables such as panel-reactive antibody (PRA) levels, donor type, and HLA mismatches in AR following renal transplantation.Material/MethodsTNF β (+252A/G), IL-10 (−592A/C), IL-1β (−511C/T) and IL-1ra (86 bp VNTR) gene polymorphisms were determined in 195 renal allograft recipients with and without AR, using PCR. Both these genotypic variants and clinical risk factors were investigated for correlation with AR within the first year after renal transplantation.ResultsPatients with increased pre-transplant PRA levels (P<0.001) and donor type (P=0.012) were prone to the development of AR. After adjusting for all variables of P<0.2, a PRA level >10% (OR=4.515, 95% confidence intervals=1.738–11.727, P=0.002) and the receipt of a graft from a donation after cardiac death (DCD) donor (OR=2.437, 95% confidence intervals=1.047–5.673, P=0.039) remained significantly associated with AR in a multivariate logistic regression analysis. No correlation could be found between recipients with an episode and absence of acute rejection and the gene polymorphisms of these cytokines investigated in the present study.ConclusionsThis study shows that the presence of increased pre-transplant levels of PRA and the receipt of a graft from DCD donor other than cytokine gene polymorphisms are significant risk factors for AR in renal transplantation. To reduce the occurrence of AR, clinicians should take necessary measures to lower the PRA levels and pay more attention to patients who received a graft from a DCD donor.

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Section: Discussionmentioning

confidence: 99%

Association Between Cytokines and Their Receptor Antagonist Gene Polymorphisms and Clinical Risk Factors and Acute Rejection Following Renal Transplantation

Xie

Wan

2016

Med Sci Monit

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“…176 Moreover, TNFR2 allele positive genotype in the donor or recipient is associated with an increased incidence of acute renal rejection. 54 Expression of TNFR2 in RAR can also be regulated by TACE, which is synthesized in situ by TECs and is colocalized with TNFR2. 177 Shedding of TNFR2 into the local environment attenuates TNF mediated inflammation.…”

Section: Kidney Transplant Rejectionmentioning

confidence: 99%

“…This is turn leads to the activation of caspase 9 and caspase 3 to initiate apoptosis. 54 Bid may also be cleaved by caspases, thus amplifying the effects of caspase 8 via caspase 9 activation. 54 TNF can also induce transcription of specific gene products that inhibit cell death by both the caspase and the JNK pathways.…”

mentioning

confidence: 99%

“…54 Bid may also be cleaved by caspases, thus amplifying the effects of caspase 8 via caspase 9 activation. 54 TNF can also induce transcription of specific gene products that inhibit cell death by both the caspase and the JNK pathways. 52 Activated NF-kB induces transcription of cFLIP (cFLICE inhibitory protein), 55 which competes with procaspase-8 binding to FADD and prevents the autocatalytic activation of caspase-8 (and -10) by the TRADD/RIPK1/ TRAF2/FADD complex.…”

mentioning

confidence: 99%

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TNF receptors: signaling pathways and contribution to renal dysfunction

Al‐Lamki

Mayadas

2015

Kidney International

170

126

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Tumor necrosis factor (TNF), initially reported to induce tumor cell apoptosis and cachexia, is now considered a central mediator of a broad range of biological activities from cell proliferation, cell death and differentiation to induction of inflammation and immune modulation. TNF exerts its biological responses via interaction with two cell surface receptors: TNFR1 and TNFR2. (TNFRs). These receptors trigger shared and distinct signaling pathways upon TNF binding, which in turn result in cellular outputs that may promote tissue injury on one hand but may also induce protective, beneficial responses. Yet the role of TNF and its receptors specifically in renal disease is still not well understood. This review describes the expression of the TNFRs, the signaling pathways induced by them and the biological responses of TNF and its receptors in various animal models of renal diseases, and discusses the current outcomes from use of TNF biologics and TNF biomarkers in renal disorders.

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“…Proinflammatory cytokine tumor necrosis factor (TNF) alpha is elevated in the serum of acutely rejecting patients [172]. Hu et al.…”

Section: Biologics In Clinical Development: Anti‐adhesion and Anti‐cymentioning

confidence: 99%

Biologics in organ transplantation

Page¹,

Dar²,

Knechtle³

2012

Transplant International

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Summary The last two decades have witnessed a pandemic in antibody development, with over 600 entering clinical studies and a total of 28 approved by the FDA and European Union. The incorporation of biologics in transplantation has made a significant impact on allograft survival. Herein, we review the armamentarium of clinical and preclinical biologics used for organ transplantation – with the exception of belatacept – from depleting and IL‐2R targeting induction agents to costimulation blockade, B‐cell therapeutics, BAFF and complement inhibition, anti‐adhesion, and anti‐cytokine approaches. While individual agents may be insufficient for tolerance induction, they provide possibilities for reduction of steroid or calcineurin inhibitor use, alternatives to rejection episodes refractory to conventional therapies, and specialized immunosuppression for highly sensitized patients.

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Donor or recipient TNF-A −308G/A polymorphism and acute rejection of renal allograft: A meta-analysis

Cited by 22 publications

References 57 publications

Association Between Cytokines and Their Receptor Antagonist Gene Polymorphisms and Clinical Risk Factors and Acute Rejection Following Renal Transplantation

Association Between Cytokines and Their Receptor Antagonist Gene Polymorphisms and Clinical Risk Factors and Acute Rejection Following Renal Transplantation

TNF receptors: signaling pathways and contribution to renal dysfunction

Biologics in organ transplantation

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