Kidney and Blood Pressure Research

Original Paper

Limited Costimulatory Molecule Expression on Renal Tubular Epithelial Cells Impairs T Cell Activation

Waeckerle-Men Y.a · Starke A.a · Wahl P.R.a · Wüthrich R.P.a, b

Author affiliations

aInstitute of Physiology and Zurich Center for Integrative Human Physiology, University of Zürich-Irchel, and bClinic for Nephrology, University Hospital Zürich, Zürich, Switzerland

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Kidney Blood Press Res 2007;30:421–429

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: May 15, 2007
Accepted: August 26, 2007
Published online: October 31, 2007
Issue release date: November 2007

Number of Print Pages: 9
Number of Figures: 6
Number of Tables: 0

ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)

For additional information: https://www.karger.com/KBR

Abstract

Background/Aims: MHC molecules are upregulated on renal proximal tubular epithelial cells (TEC) under inflammatory conditions. This allows TEC to act as ‘non-professional’ antigen-presenting cells (APC). The aim of this study was to compare the costimulatory molecule expression pattern and the T cell activation capacity between renal TEC and professional APC, e.g. bone marrow-derived dendritic cells (BM-DC). Methods: Flow cytometry analysis was used to study the costimulatory molecule surface expression on TEC or BM-DC. Ovalbumin-specific CD4 and CD8 T cell activation induced by TEC or BM-DC was compared, in terms of T cell proliferation, cytokine production and CTL activity. Results: TEC did not constitutively express significant amounts of costimulatory molecules. Stimulation of TEC with IFN-β or IFN-γ, but not other tested cytokines, enhanced the expression of PD-L1, ICOS-L and CD40. Compared to BM-DC, TEC only induced suboptimal T cell activation. Blockade of PD-L1 on both APC strongly increased T cell activity. Furthermore, high PD-L1-expressing TEC were more resistant to the cytolysis by CTL. Conclusion: The low costimulatory molecule expression may explain the suboptimal T cell activation by TEC. The IFN-upregulated negative costimulatory molecule PD-L1 on TEC may play a protective role to limit tissue injury during renal parenchymal immune responses.

© 2007 S. Karger AG, Basel




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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: May 15, 2007
Accepted: August 26, 2007
Published online: October 31, 2007
Issue release date: November 2007

Number of Print Pages: 9
Number of Figures: 6
Number of Tables: 0

ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)

For additional information: https://www.karger.com/KBR


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