Suppressed T-cell activation by IFN- -induced expression of PD-L1 on renal tubular epithelial cells

Schoop, R; Wahl, Patricia R.; Hir, Michel Le; Heemann, Uwe; Wang, Minghui; Wüthrich, Rudolf P.

doi:10.1093/ndt/gfh423

Cited by 92 publications

(82 citation statements)

References 22 publications

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“…T cells causing tubulointerstitial injury in allograft rejection [11], and also PD-L1 is strongly up-regulated by TECs in rejected kidney transplants as well as in inflamed kidneys [12][13][14]. While in the present case PD-L1 expressions in renal tubular cells were not recognized in spite of interstitial massive CD3…”

Section: Discussioncontrasting

confidence: 53%

Tubulointerstitial nephritis as adverse effect of programmed cell death 1 inhibitor, nivolumab, showed distinct histological findings

et al. 2017

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Immune-checkpoint inhibitor nivolumab (anti-PD-1 antibody) blocks T cell inhibition and stimulate immunologic response toward cancer cells. It was also revealed that PD-1/PD-L1 interaction crucially controls the effector differentiation of auto-reactive T cells to maintain self-tolerance. Therefore, potential autoimmunological side-effect can occur in any organ. Here, we report a case of 67-year-old Japanese male with lung adenocarcinoma treated with nivolumab who developed acute tubulointerstitial nephritis after the third infusion of nivolumab. Kidney biopsy showed distinct histological findings: Proliferation of CD38 positive and IgG positive plasma cells, and affluent infiltration of FoxP3? regulatory T cells. Herein, we do pathological discussion concerning acute tubulointerstitial nephritis occurred in this case based on these histological findings.

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Section: Discussioncontrasting

confidence: 53%

Tubulointerstitial nephritis as adverse effect of programmed cell death 1 inhibitor, nivolumab, showed distinct histological findings

et al. 2017

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“…We have previously shown that PD-L1 is expressed on endothelial cells and inhibits T cell activation (20). In addition, PD-L1 is expressed on microvascular endothelial cells (21,33) as well as on pancreatic islet cells (31) and tubular epithelium (34). Although we found PD-L1 in the neointima of atherosclerotic lesions, this likely reflects expression on lesional DCs or macrophages.…”

Section: Discussionmentioning

confidence: 49%

Proatherogenic immune responses are regulated by the PD-1/PD-L pathway in mice

Gotsman

Grabie²,

DaCosta³

et al. 2007

J. Clin. Invest.

187

152

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“…1D) (13,30,31). As a next step, we evaluated donor cell inhibitory signal ligands and PD-L1 expression in host tissues after BMT.…”

Section: Resultsmentioning

confidence: 99%

Programmed Death-1 Pathway in Host Tissues Ameliorates Th17/Th1-Mediated Experimental Chronic Graft-versus-Host Disease

Fujiwara

Maeda

Kobayashi

et al. 2014

The Journal of Immunology

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Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity after allogeneic hematopoietic cell transplantation, but its pathogenesis remains unclear. We investigated the role of the programmed death-1 (PD-1) pathway in chronic GVHD using a well-defined mouse model of B10.D2 (H-2d) donor to BALB/c (H-2d) recipients. PD-1 expression on allogeneic donor T cells was upregulated continuously in chronic GVHD development, whereas PD-L1 expression in host tissues was transiently upregulated and declined to basal levels in the late posttransplant period. Blockade of the PD-1 pathway by anti–PD-1, anti–PD-L1, or anti–PD-L2 mAbs exacerbated clinical and pathologic chronic GVHD. Chimeric mice revealed that PD-L1 expression in host tissues suppressed expansion of IL-17+IFN-γ+ T cells, and that PD-L1 expression on hematopoietic cells plays a role in the development of regulatory T cells only during the early transplantation period but does not affect the severity of chronic GVHD. Administration of the synthetic retinoid Am80 overcame the IL-17+IFN-γ+ T cell expansion caused by PD-L1 deficiency, resulting in reduced chronic GVHD damage in PD-L1−/− recipients. Stimulation of the PD-1 pathway also alleviated chronic GVHD. These results suggest that the PD-1 pathway contributes to the suppression of Th17/Th1-mediated chronic GVHD and may represent a new target for the prevention or treatment of chronic GVHD.

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Suppressed T-cell activation by IFN- -induced expression of PD-L1 on renal tubular epithelial cells

Cited by 92 publications

References 22 publications

Tubulointerstitial nephritis as adverse effect of programmed cell death 1 inhibitor, nivolumab, showed distinct histological findings

Tubulointerstitial nephritis as adverse effect of programmed cell death 1 inhibitor, nivolumab, showed distinct histological findings

Proatherogenic immune responses are regulated by the PD-1/PD-L pathway in mice

Programmed Death-1 Pathway in Host Tissues Ameliorates Th17/Th1-Mediated Experimental Chronic Graft-versus-Host Disease

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