Abstract
BK virus-related hemorrhagic cystitis is one of the major complications of hematopoietic stem cell transplantation. Because an immune reconstitution pattern of disease has been proposed as alternative pathogenetic model, in this study we focused on the link between BKV specific immune responses in the HSCT donor and the development of HC in paediatric HSCT recipients. We evaluated the frequency of IFN-γ-producing cells, by means of Elispot assay and flow cytometric measurement of T-cells CD8+/INFγ+, and specific cytotoxicity, in samples obtained from a cohort of 30 HLA-matched unrelated or haploidentical stem cell donors, divided into three groups, according to BKV positivity in urine and development of HC in recipients. We found that HSCT donors whose recipients developed HC have lower, though not statistically significant, levels of BKV-specific T cells, as compared with donors of recipient with isolated BK-viruria or without viruria. Although we cannot rule out that in some cases also immune reconstitution could play a role in the pathogenesis of HC, our preliminary data suggest that BKV-related HC may be related to low donor BKV-specific cytotoxic T cell transfer, perhaps coupled with impairment in BKV-specific T cell expansion posttransplant.
Highlights
Hemorrhagic cystitis (HC) is one of the major complications of hematopoietic stem cell transplantation (HSCT), causing significant morbidity and prolonged hospitalization
Support to this theory comes from the observation that HC is very rare among patients who undergo autologous as compared with allogeneic HSCT, even though similar myeloablative conditioning regimens are used, addressing the alloimmune reactions after allogeneic HSCT as an important contributing factor [19]
Most cases of postengraftment hemorrhagic cystitis occur in allogeneic HSCT with GVHD, further emphasizing the possible role of the immune system in the pathogenesis of HC [25]
Summary
Hemorrhagic cystitis (HC) is one of the major complications of hematopoietic stem cell transplantation (HSCT), causing significant morbidity and prolonged hospitalization. Based on the temporal relationship to donor stem cell engraftment, HC can be divided into two subtypes: pre-engraftment HC that occurs during or shortly after high-dose chemotherapy as part of the conditioning regimen and is related to cyclophosphamide (CY) toxicity, and post-engraftment HC which is mainly attributed to viral infections [5]. After primary infection, which is usually asymptomatic or associated with mild upper respiratory tract symptoms, BKV remains quiescent in renal tubular epithelial cells and the urothelial cell layer, and may reactivate when a natural or iatrogenic state of immunosuppression is imposed [13,14]
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