Quantitative analysis of BKV-specific CD4+ T cells before and after kidney transplantation

Mutlu, Esvet; Köksoy, Sadi; Mutlu, Derya; Yılmaz, Vural Taner; Koçak, Hüseyin; Dınçkan, Ayhan; Süleymanlar, Gültekin; Gültekin, Meral

doi:10.1016/j.trim.2015.05.005

Cited by 13 publications

(10 citation statements)

References 29 publications

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“…Our study demonstrates a substantial inverse relationship between the BK viral load and the absolute number of CD4+T cells in patients who test positive for the BK virus. In patients with BKVN nephropathy, we discovered through a study of the literature that there is a negative association between the amount of BKV-DNA and the BKV-specific CD4+T cell response [22]. Patients with bone marrow transplants exhibit a negative connection between BK virus reactivation and CD4+T cell count, which is very congruent with the findings of our study [23].…”

Section: Discussionsupporting

confidence: 90%

The change of lymphocyte subsets and inflammatory cytokine in BK viruria

Jiang,

Yuan,

Chen

et al. 2023

Preprint

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BackgroundPolyomavirus BK (BKV) infection as a serious complication after kidney transplantation. The process of infections in kidney transplant recipients is viruria, viremia, and BKVAN. The difference between BK negative and BK viruria in kidney recipients has not been defined.Patients and MethodsWe compared post-transplant lymphocyte subsets 、blood cytokines、urine cytokines levels of 19 renal transplant outpatients with (BK-positive) or without BK viruria (BK-negative, n=20), and 20 healthy controls (HCs). Group of BK-positive divide into low-(n=4) and high-level (n=15) According to BK viral load (VL).Immune cells including T cells, B cells, and natural killer (NK) cells、interleukin-2(IL-2),IL-5,IL-6, IL-1β, IL-10, IL-8, IL-17A,IL-4,IL-12P70, interferon-α(IFN-α), IFN-γ,and tumor necrosis factor-α (TNF-α)were determined by flow cytometry.ResultsBK-positive patients showed higher urine IL-1β (P=0.040), IL-10 (P=0.010), IFN-γ (P=0.002), and TNF-α (P=0.027) than BK-negative patients. Compared with HCs, BK-negative patients had lower urine IL-1β (P=0.04), IL-10 (P=0.01), TNF-α (P=0.027) and IFN-γ (P=0.004),suggesting that cytokine expression regulation BK-infection.ConclusionBK-positive renal transplant recipients, especially those with high VL, showed strong inflammatory cytokine responses with increases of urine IL-1β, IL-10, IFN-γ, and TNF-α. Our data suggest that monocyte- and Th-2-induced cytokines are involved in the pathogenesis of BKV-associated nephropathy.

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Section: Discussionsupporting

confidence: 90%

The change of lymphocyte subsets and inflammatory cytokine in BK viruria

Jiang,

Yuan,

Chen

et al. 2023

Preprint

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“…Trydzenskaya et al demonstrated that T cell stimulation using overlapping peptide pools of all five BKV antigens improved the sensitivity compared to that with single-antigen stimulation (91). This approach of using mixed peptide pools for BKV-specific T cell responses was also used by Mutlu et al to attain maximum sensitivity for the quantitation of BKV-reactive CD4 ϩ T cells prior to or following transplantation (97).…”

Section: Adaptive Immune Responsementioning

confidence: 99%

BK Polyomavirus: Clinical Aspects, Immune Regulation, and Emerging Therapies

et al. 2017

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BK polyomavirus (BKV) causes frequent infections during childhood and establishes persistent infections within renal tubular cells and the uroepithelium, with minimal clinical implications. However, reactivation of BKV in immunocompromised individuals following renal or hematopoietic stem cell transplantation may cause serious complications, including BKV-associated nephropathy (BKVAN), ureteric stenosis, or hemorrhagic cystitis. Implementation of more potent immunosuppression and increased posttransplant surveillance has resulted in a higher incidence of BKVAN. Antiviral immunity plays a crucial role in controlling BKV replication, and our increasing knowledge about host-virus interactions has led to the development of improved diagnostic tools and clinical management strategies. Currently, there are no effective antiviral agents for BKV infection, and the mainstay of managing reactivation is reduction of immunosuppression. Development of immune-based therapies to combat BKV may provide new and exciting opportunities for the successful treatment of BKV-associated complications.

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“…The late region is responsible for the production of the proteins VP1, VP2 and VP3, the role of which in BKV infection will be examined later. Finally, the non-coding control region controls the expression of the viral genes[ 423 ].…”

Section: Pathogenesis Of Bkv Infection[ 10 mentioning

confidence: 99%

“…Monitoring of both non-virus specific and virus-specific T cell responses in transplant patients has been advocated[ 405 , 417 ]. Monitoring these reponses post-transplantation may have a role in the detection of BKV reactivation[ 423 ]. T cells respond to different BKV antigens[ 419 ].…”

Section: Pathogenesis Of Bkv Infection[ 10 mentioning

confidence: 99%

BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

Vigil

Konstantinov

Barry

et al. 2016

WJT

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Nephropathy secondary to BK virus, a member of the Papoviridae family of viruses, has been recognized for some time as an important cause of allograft dysfunction in renal transplant recipients. In recent times, BK nephropathy (BKN) of the native kidneys has being increasingly recognized as a cause of chronic kidney disease in patients with solid organ transplants, bone marrow transplants and in patients with other clinical entities associated with immunosuppression. In such patients renal dysfunction is often attributed to other factors including nephrotoxicity of medications used to prevent rejection of the transplanted organs. Renal biopsy is required for the diagnosis of BKN. Quantitation of the BK viral load in blood and urine are surrogate diagnostic methods. The treatment of BKN is based on reduction of the immunosuppressive medications. Several compounds have shown antiviral activity, but have not consistently shown to have beneficial effects in BKN. In addition to BKN, BK viral infection can cause severe urinary bladder cystitis, ureteritis and urinary tract obstruction as well as manifestations in other organ systems including the central nervous system, the respiratory system, the gastrointestinal system and the hematopoietic system. BK viral infection has also been implicated in tumorigenesis. The spectrum of clinical manifestations from BK infection and infection from other members of the Papoviridae family is widening. Prevention and treatment of BK infection and infections from other Papovaviruses are subjects of intense research.

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Quantitative analysis of BKV-specific CD4+ T cells before and after kidney transplantation

Cited by 13 publications

References 29 publications

The change of lymphocyte subsets and inflammatory cytokine in BK viruria

The change of lymphocyte subsets and inflammatory cytokine in BK viruria

BK Polyomavirus: Clinical Aspects, Immune Regulation, and Emerging Therapies

BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

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