IL-2 and TNF-α Promoter Polymorphisms in Patients With Acute Kidney Graft Rejection

Pawlik, Andrzej; Domański, Leszek; Różański, Jacek; Florczak, Marcin; Dąbrowska-Żamojcin, Ewa; Dutkiewicz, Grażyna; Gawrońska-Szklarz, B

doi:10.1016/j.transproceed.2005.03.091

Cited by 31 publications

(17 citation statements)

References 15 publications

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“…T lymphocytes play an important role in the development of acute kidney allograft rejection [16] and VEGF is an important molecule in the dialogue between transplanted tissues and the immune system [17]. Mor et al reported that antigen-stimulated T cells secrete VEGF in vitro and that T cells migrating into the inflammation sites provide a source of VEGF [6].…”

Section: Discussionmentioning

confidence: 99%

VEGF 936 C/T gene polymorphism in renal transplant recipients: Association of the T allele with good graft outcome

et al. 2007

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Section: Discussionmentioning

confidence: 99%

VEGF 936 C/T gene polymorphism in renal transplant recipients: Association of the T allele with good graft outcome

et al. 2007

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“…17,18 Additionally, no relevant association was observed between gene polymorphisms and IL-2 production and graft rejection in kidney and heart transplant recipients. 19,20 Genetic polymorphism analysis related to high-or low-cytokine production and activity may indicate a genetic predisposition associated with acute rejection and clinical outcome, but data so far are inconclusive. The discrepancies between studies may be partly explained by differing levels of immunosuppression and ethnic variations in studied populations.…”

Section: Introductionmentioning

confidence: 99%

T-Cell Cytokines as Predictive Markers of the Risk of Allograft Rejection

Brunet

López

López-Hoyos

2016

Therapeutic Drug Monitoring

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Over the last decade, several biomarkers and surrogate markers have surfaced as promising predictive markers of risk of rejection in solid organ transplantation. The monitoring of these markers can help to improve graft and recipient care by personalizing immunomodulatory therapies. The complex immune system response against an implanted graft can change during long-term follow-up, and the dynamic balance between effector and regulatory T-cell populations is a crucial factor in antidonor response, risk of rejection, and immunosuppression requirements. Therefore, at any time before and after transplantation, T-effector activity, which is associated with increased production and release of proinflammatory cytokines, can be a surrogate marker of the risk of rejection and need for immunosuppression. In addition, immunosuppressive drugs may have a different effect in each individual patient. The pharmacokinetics and pharmacodynamics of these drugs show high interpatient variability, and pharmacodynamic markers, strongly associated with the specific mechanism of action, can potentially be used to measure individual susceptibility to a specific immunosuppressive agent. The monitoring of a panel of valid biomarkers can improve patient stratification and the selection of immunosuppressive drugs. After transplantation, therapy can be adjusted based on the prediction of rejection episodes (maintained alloreactivity), the prognosis of allograft damage, and the individual's response to the drugs. This review will focus on current data indicating that changes in the T-cell production of the intracellular cytokines interferon-γ and interleukin-2 could be used to predict the risk of rejection and to guide immunosuppressive therapy in transplant recipients.

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“…T lymphocytes play an important role in the development of acute kidney allograft rejection [20]. Mor et al [21] reported that antigen-stimulated T cells secrete VEGF in vitro and that T cells migrating to the inflammation sites provide a source of VEGF (fig.…”

Section: Discussionmentioning

confidence: 99%

Impact of Vascular Endothelial Growth Factor Single Nucleotide Polymorphism Association on Acute Renal Allograft Rejection

Prakash

Agrawal

Kumar

et al. 2015

Nephron

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Background: Vascular endothelial growth factor (VEGF) is a cytokine which plays an important role in the division, proliferation and migration of endothelial cells. In the kidney, VEGF expression is found in glomerular podocytes and in tubular epithelial cells, which may result in acute inflammatory reactions. Methods: The role of VEGF gene polymorphisms (-2578 C/A, -2549 18 bp Ins/Del, -1154 G/A and +936 C/T) was investigated in 272 patients who underwent renal transplantation. ARMS-PCR and PCR-RFLP were used. Patients were categorized into acute allograft rejection (n = 76) and nonrejection (n = 196). Results: The VEGF -1154 GG genotype and the +936 T allele were found to be susceptible to acute rejection (AR). T-A-A-I, T-A-A-D, T-G-C-I and C-A-A-I haplotypes revealed a predisposition among AR cases. In silico analysis revealed +936 T as a significant allele involved in the transcription regulation. Conclusion: These results highlight the role of VEGF polymorphisms in acute allograft rejection.

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IL-2 and TNF-α Promoter Polymorphisms in Patients With Acute Kidney Graft Rejection

Cited by 31 publications

References 15 publications

VEGF 936 C/T gene polymorphism in renal transplant recipients: Association of the T allele with good graft outcome

VEGF 936 C/T gene polymorphism in renal transplant recipients: Association of the T allele with good graft outcome

T-Cell Cytokines as Predictive Markers of the Risk of Allograft Rejection

Impact of Vascular Endothelial Growth Factor Single Nucleotide Polymorphism Association on Acute Renal Allograft Rejection

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