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The Loss of BKV‐specific Immunity From Pretransplantation to Posttransplantation Identifies Kidney Transplant Recipients at Increased Risk of BKV Replication
Author(s) -
Schachtner T.,
Stein M.,
Babel N.,
Reinke P.
Publication year - 2015
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/ajt.13252
Subject(s) - immunosuppression , elispot , bk virus , medicine , immunology , virology , viral replication , immunity , kidney transplantation , interferon , immune system , cd8 , transplantation , virus
Quantification of BKV‐load and BKV‐specific immunity have been evaluated to monitor BKV‐replication and outcomes in kidney transplant recipients (KTRs) with BKV‐infection. However, it remains crucial to better understand how immune markers can predict the risk for later infection. We studied all KTRs between 2008 and 2011. Twenty‐four KTRs were diagnosed with BKV‐replication and a control group of 127 KTRs was used for comparison. Samples were collected before at +1, +2, and +3 months posttransplantation. BKV‐specific and alloreactive T cells were measured using an interferon‐γ Elispot assay. The extent of immunosuppression was quantified by lymphocyte subpopulations and interferon‐gamma levels. KTRs with a loss of BKV‐specific T cells directed to Large T‐antigen from pretransplantation to posttransplantation were at increased risk of BKV‐replication (p < 0.001). In contrast, KTRs with stable/rising BKV‐specific T cells were more likely not to develop BKV‐replication (p < 0.05). KTRs developing BKV‐replication showed significantly lower CD3+, CD4+, CD8+ T cells and interferon‐γ levels posttransplantation, but significantly higher alloreactive T cells (p < 0.05). Monitoring pretransplant and posttransplant BKV‐specific T cells is suggested a sensitive marker to identify KTRs at increased risk of BKV‐replication. Increased susceptibility to immunosuppression predisposes KTRs to a loss of protective BKV‐specific immunity that results in impaired virus control and BKV‐replication.