Polyomavirus BK-specific cellular immune response to VP1 and large T-antigen in kidney transplant recipients
- PMID: 17359507
- DOI: 10.1111/j.1600-6143.2007.01754.x
Polyomavirus BK-specific cellular immune response to VP1 and large T-antigen in kidney transplant recipients
Abstract
Polyomavirus BK (BKV) is the primary cause of polyomavirus-associated nephropathy (PVAN) in kidney transplant (KT) recipients. Using ELISpot assays, we compared the frequency of interferon-gamma (IFN-gamma) secreting peripheral blood mononuclear cells (PBMC) after stimulation with overlapping peptide pools covering BKV large T-antigen (LT) and VP1 capsid proteins (VP1). In 10 healthy donors, LT and VP1 responses were low with median 24 (range 15-95) and 25 (7-113) spot-forming units/10(6) PBMC (SFU), respectively. In 42 KT patients with current or recent plasma BKV loads, median LT and VP1 responses of 29 (0-524) and 114 (0-1432) SFU were detected, respectively. In KT patients with decreasing or past plasma BKV loads, significantly higher median BKV-specific IFN-gamma responses were detected compared to KT patients with increasing or persisting BKV loads [LT: 78 (8-524) vs. 22 (0-120) SFU, p=0.003; VP1: 285 (45-1432) vs. 53 (0-423) SFU, p=0.001, respectively]. VP1-specific IFN-gamma responses were higher and more likely to involve CD4(+) T cells, while CD8(+) T cells were more frequently directed against LT. Stimulation with JCV-specific VP1 and LT peptides indicated only low-level cross-recognition. The data suggest that control of BKV replication is correlated with differentiated expansion of BKV-specific cellular immune responses.
Comment in
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BK viral loads and immune monitoring in renal transplant recipients.Am J Transplant. 2007 May;7(5):1039-40. doi: 10.1111/j.1600-6143.2007.01767.x. Am J Transplant. 2007. PMID: 17456195 No abstract available.
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