Predominance of Th2 cells and plasma cells in polyoma virus nephropathy: a role for humoral immunity?

Buettner, Maike; Xu, Hui; Böhme, Romy; Seliger, Barbara; Jacobi, Johannes; Wiesener, Michael S.; Benz, Kerstin; Amann, Kerstin

doi:10.1016/j.humpath.2011.11.006

Cited by 12 publications

(11 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…T lymphocyte depletion by immunosuppressive medications may lead to Th2 pathway activation leading to B lymphocyte and plasma cell rich infiltrations seen in BKVN. 29 In a similar vein, significantly reduced Natural Killer (NK) cell function was documented in RTR with BKVN by Trydzenskaya et al, 30 highlighting the impaired host defence. They demonstrated in 48 patients with BKVN with 110 normal RTR as controls that activating NK cell Iglike receptors showed lower frequency.…”

Section: Bk Virus Nephropathymentioning

confidence: 75%

“…In a study of 30 biopsies‐12 with BKVN, 12 with ACR and six controls, they noted that the range of Foxp 3 staining was larger (0–270) compared with ACR (0–35) although it did not reach significance because of overlap. T lymphocyte depletion by immunosuppressive medications may lead to Th2 pathway activation leading to B lymphocyte and plasma cell rich infiltrations seen in BKVN . In a similar vein, significantly reduced Natural Killer (NK) cell function was documented in RTR with BKVN by Trydzenskaya et al ., highlighting the impaired host defence.…”

Section: Bk Virus Nephropathymentioning

confidence: 80%

See 1 more Smart Citation

BK virus nephropathy in renal transplant recipients

Jamboti

2016

Nephrology

View full text Add to dashboard Cite

ABSTRACT:BK virus nephropathy (BKVN) occurs in up to 10% of renal transplant recipients and can result in graft loss. The reactivation of BK virus in renal transplant recipients is largely asymptomatic, and routine surveillance especially in the first 12-24 months after transplant is necessary for early recognition and intervention. Reduced immunosuppression and anti-viral treatment in the early stages may be effective in stopping BK virus replication. Urinary decoy cells, although highly specific, lack sensitivity to diagnose BKVN. Transplant biopsy remains the gold standard to diagnose BKVN, good surrogate markers for surveillance using quantitative urinary decoy cells, urinary SV40 T immunochemical staining or polyoma virus-Haufen bodies are offered by recent studies. Advanced BKVN results in severe tubulo-interstitial damage and graft failure. Retransplantation after BKVN is associated with good outcomes. Newer treatment modalities are emerging.

show abstract

Section: Bk Virus Nephropathymentioning

confidence: 75%

Section: Bk Virus Nephropathymentioning

confidence: 80%

BK virus nephropathy in renal transplant recipients

Jamboti

2016

Nephrology

View full text Add to dashboard Cite

show abstract

“…We and others have recently described plasma cell infiltrates in renal allografts of patients with PyVAN suggesting that humoral immunity may play a role in polyoma viral disease [22,23], and it is intriguing to speculate that the use of rituximab may modulate the risk for PyVAN. However, in our study neither the use of ATG or rituximab given within the first year after transplantation was associated with BK viremia.…”

Section: Discussionmentioning

confidence: 99%

BK viremia and polyomavirus nephropathy in 352 kidney transplants; risk factors and potential role of mTOR inhibition

et al. 2013

Self Cite

View full text Add to dashboard Cite

BackgroundPolyomavirus BK nephropathy (PyVAN) remains an important cause of early graft dysfunction and graft loss in kidney transplantation.MethodsIn this retrospective, single centre cohort study we studied the incidence and outcome of BK viral infection in 352 patients transplanted in 2008–2011.ResultsDuring follow-up viral replication was detected in 48 patients (13.6%); 22 patients (6.2%) had biopsy proven PyVAN.In multivariate logistic regression analyses risk factors for BK-viremia were lack of enrolment into randomized controlled trials (RCTs), biopsy proven acute rejections, cytomegaly virus (CMV) serostatus of both donor and recipient and previous transplantation.In patients without PyVAN reduction or switch of immunosuppression was associated with rapid viral clearance and stable graft function. In contrast, in most patients with PyVAN graft function deteriorated and 5 patients prematurely lost their allograft. Switch of immunosuppression to a low dose cyclosporine plus mTOR inhibitor based regimen in patients with PyVAN was safe, well tolerated and tended to be associated with a better short-term outcome in terms of graft function compared to reduction of existing immunosuppression alone.ConclusionsWith the lack of licensed anti-polyoma viral drugs reduction or conversion of immunosuppression remains the mainstay of therapy in patients with PyVAN. The combination of low dose cyclosporine plus mTOR inhibition appears to be safe and warrants further investigation.

show abstract

“…Some studies have reported a significant increase in B cells and plasma cells in BKPyVAN, 3,6,8,23 whereas other studies did not find any differences in cell counts. 7,24 In our study, we show that the amount of T cells (in multivariable analyses), B cells, and plasma cells is comparable during BKPyVAN and TCMR as well as after we corrected the cell counts for the degree of total inflammation in the biopsy.…”

Section: Discussionmentioning

confidence: 90%

“…Some studies reported the presence of more B lymphocytes in BKPyVAN, [3][4][5][6] whereas others found no differences in the amount of T and B cells. 7 Buettner et al 8 showed a higher number of plasma cells in BKPyVAN compared with TCMR. The demonstration of lymphocytic infiltrates, marked tubulitis, and tubular HLA-DR expression in areas lacking polyomavirus replication may support the diagnosis of TCMR as proposed by Nickeleit et al 9 ; however, the former two criteria are often observed in BKPyVAN as well and therefore, cannot be considered pathognomic.…”

mentioning

confidence: 98%

Intragraft Blood Dendritic Cell Antigen-1–Positive Myeloid Dendritic Cells Increase during BK Polyomavirus–Associated Nephropathy

Yapici¹,

Kers²,

Slavujevic-Letic³

et al. 2015

JASN

View full text Add to dashboard Cite

Although both polyomavirus infection and T cell-mediated rejection (TCMR) are characterized by tubulointerstitial inflammation in the renal allograft, these conditions are treated with opposing therapeutic regimens. To gain more insight into the differences between antiviral and alloimmune responses, we performed a case-control study, in which we immunophenotyped the inflammatory infiltrates in renal biopsy specimens with BK polyomavirus-associated nephropathy (BKPyVAN) and specimens with TCMR. Compared with TCMR, BKPyVAN was diagnosed later after transplantation; therefore, BKPyVAN specimens showed more chronic damage than TCMR specimens showed. However, TCMR and BKPyVAN specimens had comparable levels of tubulointerstitial inflammation. Adjustment for confounders in various multivariable models revealed more blood dendritic cell antigen-1 + (BDCA-1 + ) myeloid dendritic cells (mDCs) present during BKPyVAN (odds ratio, 2.31; 95% confidence interval, 1.03 to 5.16; P=0.04) than during TCMR. Double immunostaining for SV40 and BDCA-1 showed that, during BKPyVAN, BDCA-1 + mDCs localized in proximity to the polyomavirus-infected tubular epithelial cells. We ensured that time of biopsy after transplantation was not a confounding factor by including additional specimens with late TCMR and protocol biopsy specimens matched for biopsy time. These additional specimens showed amounts of BDCA-1 + mDCs comparable with amounts in the early TCMR specimens. These results suggest that BDCA-1 + mDCs, known to be involved in the antiviral immune response during various viral infections, might have a pivotal role during BKPyVAN infection in the grafted kidney.

show abstract

Predominance of Th2 cells and plasma cells in polyoma virus nephropathy: a role for humoral immunity?

Cited by 12 publications

References 35 publications

BK virus nephropathy in renal transplant recipients

BK virus nephropathy in renal transplant recipients

BK viremia and polyomavirus nephropathy in 352 kidney transplants; risk factors and potential role of mTOR inhibition

Intragraft Blood Dendritic Cell Antigen-1–Positive Myeloid Dendritic Cells Increase during BK Polyomavirus–Associated Nephropathy

Contact Info

Product

Resources

About