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Kidney transplant recipients with persistent BK polyomavirus (BKPyV) DNAemia show exhausted T cells. Blocking PD1 and TIM3 pathways restored BKPyV-specific CD8 T-cell functions, suggesting new therapeutic strategies.

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Area of Science:

  • Immunology
  • Transplantation
  • Virology

Background:

  • BK polyomavirus (BKPyV) nephropathy is a major cause of graft loss in kidney transplant recipients.
  • Current treatment involves reducing immunosuppression to control BKPyV replication.

Purpose of the Study:

  • To investigate the T-cell response in kidney transplant recipients with BKPyV DNAemia.
  • To identify factors associated with treatment response and explore novel therapeutic targets.

Main Methods:

  • Analysis of circulating T cells from 28 kidney transplant recipients with BKPyV DNAemia.
  • Evaluation of BKPyV-specific T-cell functionality, phenotype, and graft outcomes.
  • Assessment of T-cell inhibitory receptor expression and ex vivo T-cell function restoration.

Main Results:

  • Patients with sustained BKPyV DNAemia (noncontrollers) exhibited impaired BKPyV-specific T-cell function and an exhausted phenotype.
  • Impaired T-cell function was linked to overexpression of inhibitory receptors like PD1 and TIM3.
  • Combination therapy with anti-PD1 and anti-TIM3 antibodies restored BKPyV-specific CD8 T-cell functions ex vivo.

Conclusions:

  • Sustained BKPyV DNAemia in kidney transplant recipients is associated with T-cell exhaustion.
  • Targeting PD1 and TIM3 pathways offers a promising strategy for restoring anti-BKPyV T-cell immunity.