Immunocheckpoint Modulation of PD-L1/PD-1 as a Novel Therapeutic Strategy Against Peritoneal Dialysis-Associated Fibrosis

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Immunocheckpoint Modulation of PD-L1/PD-1 as a Novel Therapeutic Strategy Against Peritoneal Dialysis-Associated Fibrosis

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Co-author 1

Lijie He helijie@fmmu.edu.cn Xijing Hospital, The Fourth Military Medical University Department of Nephrology Xi’an China *

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Yuting Zhang zhangyuting_51@163.com Xijing Hospital, The Fourth Military Medical University Department of Nephrology Xi’an China -

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Introduction

In long-term peritoneal dialysis patients, the decline in peritoneal function and peritoneal fibrosis represent one of the major causes of peritoneal dialysis failure. The presence of a T-cell-mediated microinflammatory state promotes the progression of peritoneal fibrosis, and T-cell activation affecting immune checkpoints may play a critical regulatory role in this process.

Methods

We enrolled peritoneal dialysis patients and grouped them by dialysis duration. Serum sPD-1 levels were measured. A peritoneal fibrosis mouse model was established to correlate serum sPD-1 levels with fibrosis severity. The functional impact of sPD-1 was confirmed by administering it to model mice. Furthermore, exogenous PD-L1 fusion protein was administered to neutralize sPD-1. Mechanistic studies were conducted on human peritoneal mesothelial cells to examine the effect of sPD-1 on PD-L1 internalization and epithelial-mesenchymal transition (EMT).

Results

Long-term peritoneal dialysis patients exhibited elevated serum sPD-1 levels. In the animal model, high sPD-1 levels correlated with the degree of peritoneal fibrosis. Administration of sPD-1 exacerbated fibrosis in mice, while supplementation with PD-L1 fusion protein alleviated it. In vitro, sPD-1 bound to PD-L1 on human peritoneal mesothelial cells, mediating its internalization and recycling, leading to PD-L1 upregulation on the cell surface and promoting EMT.

Conclusion

This study elucidates the role of sPD-1 in peritoneal fibrosis within the context of peritoneal microinflammation, filling a gap in understanding how sPD-1 promotes EMT in this inflammatory milieu. It refines the theory of sPD-1-mediated fibrosis and provides new perspectives and directions for targeting peritoneal function protection. In terms of potential applications, this research establishes a solid theoretical foundation for developing new therapeutic strategies for peritoneal fibrosis.

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