Natural killer cell response to BK virus infection in polyoma virus–associated nephropathy of renal transplant recipients

Acott, Philip D.

doi:10.1038/ki.2013.148

Cited by 7 publications

(8 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…19 In ammatory NK-cell antiviral responses involve interactions between activation receptors, such as killer-cell immunoglobulin-like receptors (KIRs), and host-cell MHC class I molecules, which alters cell sensitivity to lysis by NK cells. 20 After KT, the ischemic injury may reactivate BKPyV from the allograft kidney and trigger the innate immune system shortly after allograft reception. NK cells recognize virus-infected cells through the downregulation of MHC class I and inhibitory receptors as well as via the upregulation of activator molecules 19 .…”

Section: Discussionmentioning

confidence: 99%

Clinical and Immunological Characteristics for BK Polyomavirus- associated Nephropathy after Kidney Transplantation

Siripoon

Apiwattanakul

Mongkolrattanakul

et al. 2022

Preprint

View full text Add to dashboard Cite

Background BK polyomavirus (BKPyV)-associated nephropathy (BKPyVAN) could cause allograft dysfunction among kidney transplant (KT) recipients. Intact BKPyV-specific immunity is correlated with viral containment, therefore clinical and immunological characteristics related to BKVAN after KT needs to be explored. Methods We prospectively investigated an association between clinical baseline characteristics, BK polyomavirus (BKPyV)-specific immunity, and BKPyV-associated nephropathy (BKPyVAN) in KT recipients. BKPyV-specific immunity, measured with intracellular cytokine assays, is reported as the percentage of IFN-γ-producing CD4+ T, CD8+ T, natural killer (NK), and NKT cells after large-T antigen and viral capsid protein 1 (VP1) stimulation. Results Among 100 KT patients, BKPyVAN occurred in 18% within one-year post-KT. There were 70 patients (70%) who received an induction immunosuppressive therapy. Diabetic nephropathy was significantly associated with BKPyVAN. Among 40 patients who were eligible for the immunological study. In a multivariate analysis, pre-KT %VP1-specific NK cells were independently associated with BKPyVAN (HR, 1.209; 95%CI, 1.055–1.386; P = 0.006). In those with BKPyVAN, the mean %NK (coefficient, 1.202; 95%CI, 0.033–2.371; P = 0.04), %VP1-specific NK (coefficient, 2.602; 95%CI, 1.083–4.121; P = 0.001), and %NKT (coefficient, 0.199; 95%CI, 0.051–0.348; P = 0.008) cells at 1-month post-KT were significantly higher than those pre-KT. Thus, increasing NK, VP1-specific NK, and NKT cell proportions were observed among KT recipients who developed BKPyVAN within the first year. Conclusion KT recipients with underlying diabetes and the presence of BKPyV-specific NK- and NKT-cell immunity could be at risk of BKPyVAN after KT. BKPyV-specific innate immune monitoring could potentially stratify those at risk of BKPyVAN among KT recipients. (Thai Clinical Trials Registry, TCTR20190404004)

show abstract

Section: Discussionmentioning

confidence: 99%

Clinical and Immunological Characteristics for BK Polyomavirus- associated Nephropathy after Kidney Transplantation

Siripoon

Apiwattanakul

Mongkolrattanakul

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Binding of BKPyV peptides to HLA class I alleles, presentation of BKPyV antigens, and initiation of cytotoxic T cell–mediated immune response were demonstrated in experimental studies 20,21 . Additionally, HLA class I molecules play a pivotal role in activity of NK cells against BKPyV through killer‐cell immunoglobulin‐like receptors (KIRs) 8 . Specific HLA class I antigens such as HLA‐B51 have been shown to provide protective effects against BKPyV DNAemia 22 .…”

Section: Discussionmentioning

confidence: 99%

“…Human leukocyte antigen (HLA) class I presentation pathway plays a central role in alerting the immune system to virally infected cells 6,7 . Recognition of HLA class I molecules is required for the activation of natural killer (NK) cells through killer‐cell immunoglobulin‐like receptors (KIRs) 8,9 . HLA class I molecules play a considerable role in KIR interaction and lysis of renal tubular epithelial cells infected with BKPyV 8 .…”

Section: Introductionmentioning

confidence: 99%

“…Recognition of HLA class I molecules is required for the activation of natural killer (NK) cells through killer‐cell immunoglobulin‐like receptors (KIRs) 8,9 . HLA class I molecules play a considerable role in KIR interaction and lysis of renal tubular epithelial cells infected with BKPyV 8 . Additionally, CD8+ T cells recognizing HLA class I antigens eliminate virally infected cells.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 HLA class I molecules play a considerable role in KIR interaction and lysis of renal tubular epithelial cells infected with BKPyV. 8 Additionally, CD8+ T cells recognizing HLA class I antigens eliminate virally infected cells. Thus, HLA class I appears to be critically important in recognition of BKPyV-infected cells by NK cells through KIRs and cytotoxic T cells.…”

mentioning

confidence: 99%

See 2 more Smart Citations

The effect of human leukocyte antigen A1 and B35‐Cw4 on sustained BK polyomavirus DNAemia after renal transplantation

Hosseini-Moghaddam

Jevnikar

et al. 2020

Clinical Transplantation

View full text Add to dashboard Cite

BK polyomavirus (BKPyV) is a known cause of nephropathy in renal allograft recipients. Reactivation of latent BKPyV infection causes significant viruria in 30%-40% of renal transplant patients. 1,2 Subsequently, one third of patients with BKPyV viruria develop DNAemia, which indicates more extensive replication and damage to the allograft. 3 BKPyV DNAemia may progress to significant fibrosis of the renal allograft and tubular atrophy known as polyomavirus-associated nephropathy (PyVAN). 3,4 PyVAN is unfortunately associated with 10%-100% graft loss rate. 5,6 Human leukocyte antigen (HLA) class I presentation pathway plays a central role in alerting the immune system to virally infected cells. 6,7 Recognition of HLA class I molecules is required for the

show abstract

Clinical and immunological characteristics for BK polyomavirus‐associated nephropathy after kidney transplantation

Siripoon,

Apiwattanakul,

Mongkolrattanakul

et al. 2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

IntroductionBK polyomavirus (BKPyV)‐associated nephropathy (BKPyVAN) can cause a significant risk of allograft impairment after kidney transplantation (KT). Intact BKPyV‐specific immunity is associated with viral containment. This study investigated BKPyV‐specific immunological factors among KT recipients.MethodsThis prospective study in a single transplant center from January 2019 to August 2019 assessed associations between clinical and immunological characteristics, with a focus on BKPyV‐cell‐specific immunity and BKPyVAN, among KT recipients aged ≥15 years. The numbers of interferon‐gamma (IFN‐γ)‐producing CD4+ T, CD8+ T, natural killer (NK), and natural killer T (NKT) cells were measured after stimulation with large T antigen and viral capsid protein 1 (VP1).ResultsIn total, 100 KT recipients were included (mean age ± SD, 42 ± 11 years); 35% of the recipients were female patients, and 70% had received induction immunosuppressive therapy. The 1‐year cumulative incidence of high‐level BKPyV DNAuria (possible BKPyVAN) and (presumptive BKPyVAN) was 18%. Among 40 patients with immunological factor data, pre‐KT %NK cells (hazard ratio [HR], 1.258; 95% confidence interval [CI], 1.077–1.469; p = .004) and %VP1‐specific NK cells (HR, 1.209; 95% CI, 1.055–1.386; p = .006) were factors independently associated with possible and presumptive BKPyVAN. KT recipients with possible and presumptive BKPyVAN were more likely to exhibit significant mean coefficients of %NK, %VP1‐specific NK, and %NKT cells at 1 month after KT than before KT (all p < .05).ConclusionIndividuals with nonspecific and VP1‐specific NK cells before KT and increasing numbers of these cells after KT may be at risk for high‐level BKPyV DNAuria and presumptive BKPyVAN. Further studies are needed to determine the utility of BKPyV‐specific innate immune surveillance in predicting the occurrence of BKPyVAN.

show abstract

Natural killer cell response to BK virus infection in polyoma virus–associated nephropathy of renal transplant recipients

Cited by 7 publications

References 16 publications

Clinical and Immunological Characteristics for BK Polyomavirus- associated Nephropathy after Kidney Transplantation

Clinical and Immunological Characteristics for BK Polyomavirus- associated Nephropathy after Kidney Transplantation

The effect of human leukocyte antigen A1 and B35‐Cw4 on sustained BK polyomavirus DNAemia after renal transplantation

Clinical and immunological characteristics for BK polyomavirus‐associated nephropathy after kidney transplantation

Contact Info

Product

Resources

About