AI Article Synopsis
- Chemokines and their receptors are important in immunity and inflammation, and this study investigates their impact on kidney transplant rejection.
- The study involved 100 donor-recipient pairs, evaluating two gene polymorphisms, CCR2-V64I and CCR5-Delta32, using genetic testing methods but found no significant relationships to acute rejection (AR) or delayed graft function (DGF).
- Although no strong associations were found between the gene polymorphisms and transplant outcomes, factors like the cause of kidney failure and donor-recipient sex matching showed weak links to AR and DGF, highlighting the importance of considering these in transplant situations.
Article Abstract
Introduction: Chemokines and chemokine receptors have a pivotal role in immunity and inflammation. We aimed to evaluate their role in kidney transplant rejection.
Materials And Methods: The association of chemokine (C-C motif) receptor 2 (CCR2)-V64I and CCR5-Delta32 gene polymorphisms with acute rejection (AR) and delayed graft function (DGF) were examined in 100 donor-recipient pairs. The CCR2-V64I and CCR5-Delta32 alleles were determined using polymerase chain reaction and polymerase chain reaction-restriction fragment length polymorphism, respectively.
Results: No associations were found between donors or recipients' CCR2-V64I and CCR5-Delta32 gene polymorphisms and AR or DGF. Of the characteristics of the donors, recipients, and transplantation, glomerulonephritis as a cause of kidney failure in the recipients was weakly associated with AR (relative risk, 6.1; 95% confidence interval, 0.8 to 46.0; P = .07). Transplantation of kidney from females to males was weakly associated with DGF (relative risk, 5.5; 95% confidence interval, 0.9 to 33.0; P = .06). There was a significant association between AR, but not DGF, and graft loss in the patients (relative risk, 28.6; 95% confidence interval, 1.7 to 487.0; P = .03).
Conclusions: Our study failed to suggest CCR2-V64I or CCR5-Delta32 gene polymorphisms as risk factors for AR and DGF in kidney transplantation. Sex-matching between donors and recipients should be considered for living donor kidney transplantation.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Association between chemokine genes polymorphisms and susceptibility to Parkinson's disease: a meta-analysis and systematic review.
Acta Neurol Belg
July 2024
Department of Rheumatology, Korea University Anam Hospital, Korea University College of Medicine, 73, Goryeodae-ro, Seongbuk-gu, Seoul, 02841, Korea.
Objective: This study aimed to investigate the potential association between polymorphisms in monocyte chemoattractant protein-1 (MCP-1), chemokine receptor type 2 (CCR2), type 5 (CCR5), regulated on activation, normal T cell expressed, and secreted (RANTES) and susceptibility to Parkinson's disease (PD).
Methods: The MEDLINE, EMBASE, and Web of Science databases were searched for relevant articles, and a meta-analysis was conducted to assess the associations between the MCP-1 -2518 G/A, CCR2 V64I, CCR5-Δ32, RANTES - 405 G/A, -28 G/A polymorphisms and the risk of PD.
Results: Six studies with 1,416 patients with PD and 1,715 controls that met the inclusion criteria were identified.
Effect of Chemokine Gene Variants on Covid-19 Disease Severity.
Immunol Invest
October 2022
Istanbul Faculty of Medicine, Department of Medical Biology, Istanbul University, Istanbul, Turkey.
Patients immune phenotype/genotype data may be useful to understand the molecular mechanisms involved in SARS-CoV-2 infection and can contribute to the identify the different levels of disease severity. The roles of chemokines have been reported in the coronavirus-related diseases SARS and MERS and they may likewise play a critical role in the development of the symptoms of COVID-19 disease. We analyzed the association of the MCP-1-A2518 G, SDF-1-3'A, CCR5-delta32, CCR5-A55029 G, CXCR4-C138T and CCR2-V64I gene polymorphisms with COVID-19 severity to further unveil the immunological pathways leading to disease severity and death.
View Article and Find Full Text PDFA Case-Control Association Study of -28> Polymorphism as a Risk Factor for Parkinson's Disease in Isparta, Turkey.
Parkinsons Dis
December 2016
Department of Medical Biology, Faculty of Medicine, Süleyman Demirel University, Isparta, Turkey.
. Recent studies have revealed that inflammatory processes are involved in the pathogenesis of Parkinson's disease (PD). Multiple lines of evidence have suggested that chemokines and their receptors are involved in several neurodegenerative disorders.
View Article and Find Full Text PDFChemokine and Chemokine Receptor Polymorphisms in Bipolar Disorder.
Psychiatry Investig
September 2016
Department of Neuroscience, Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey.
Objective: Bipolar disorder (BD) is a debilitating psychiatric disease with unknown etiology. Recent studies have shown inflammation as a potential contributing factor of BD pathogenesis. However, potential associations between chemokine and chemokine receptor polymorphisms and BD have been fundamentally understudied.
View Article and Find Full Text PDFChemokine gene variants in schizophrenia.
Nord J Psychiatry
August 2016
a Department of Molecular Medicine , Institute of Experimental Medicine, Istanbul University, Istanbul , Turkey ;
Background Chemokines are known to play a major role in driving inflammation and immune responses in several neuroinflammatory diseases, including multiple sclerosis, Alzheimer's disease and Parkinson's disease. Inflammation has also been implicated in the pathogenesis of schizophrenia. Aim We aimed to investigate a potential link between chemokines and schizophrenia and analyze the role of MCP-1-A2518G, SDF-1-3'A, CCR5-delta32, CCR5-A55029G, CXCR4-C138T and CCR2-V64I gene polymorphisms in the Turkish population.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!