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Abstract: FR-PO691

CD4+ T Cell Egress in Crescentic Glomerulonephritis Is Regulated by a Converse Expression of S1PR1 and CXCR6

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis


  • Engeßer, Jonas, Universitatsklinikum Hamburg-Eppendorf, Hamburg, Hamburg, Germany
  • Paust, Hans-Joachim, Universitatsklinikum Hamburg-Eppendorf, Hamburg, Hamburg, Germany
  • Zhao, Yu, Universitatsklinikum Hamburg-Eppendorf Zentrum fur Molekulare Neurobiologie Hamburg, Hamburg, Germany
  • Meyer-Schwesinger, Catherine, Universitatsklinikum Hamburg-Eppendorf, Hamburg, Hamburg, Germany
  • Wiech, Thorsten, Universitatsklinikum Hamburg-Eppendorf, Hamburg, Hamburg, Germany
  • Bonn, Stefan, Universitatsklinikum Hamburg-Eppendorf Zentrum fur Molekulare Neurobiologie Hamburg, Hamburg, Germany
  • Krebs, Christian F., Universitatsklinikum Hamburg-Eppendorf, Hamburg, Hamburg, Germany
  • Panzer, Ulf, Universitatsklinikum Hamburg-Eppendorf, Hamburg, Hamburg, Germany

Group or Team Name

  • Panzer Lab.

Autoimmune diseases such as crescentic glomerulonephritis (cGN) are characterized by a dramatically increased migration of leukocytes to the inflamed tissue. Infiltration of CD4+ T cells play a key role in orchestrating the immune response during inflammation. However, little is known about the function and mechanisms of T cell exit out of the kidney. The aim of this study is to characterize the CD4+ T cell retention and emigration receptors and their implication on tissue injury, especially in the context of restitutio vs chronification of tissue inflammation.


Lymph vessel staining of renal biopsy cores was performed by immunohistochemistry (IHC). For leukocyte trafficking analysis cGN was induced in Kaede-mice, ubiquitously expressing the photoconvertible Kaede protein. Photoconversion of intrarenal leukocytes was performed by UV-A light (385 nm) exposure of the left kidney. Leukocytes from kidneys, blood and dLN were analyzed by scRNAseq, flow-cytometry and IHC. For analysis of the chemokine receptor CCR7 a CCR7-/- deficient mouse model was used, for analysis of CXCR6 a depleting antibody of its sole ligand CXCL16 was used. S1PR1 signaling was blocked using FTY720.


In human biopsy cores an exit of CD4+ T cells but not CD68+ macrophages via the lymphatics could be shown. Murine analysis of emigrated CD4+ T cells revealed a set of differentially expressed genes compared to resident CD4+ T cells, mainly a downregulation of the chemokine receptor CXCR6 and an upregulation of S1PR1. CCR7, although upregulated on CD4+ T cells showed to be dispensable for T cell egress. Depleting CXCL16 resulted in an increased migration of CD4+ T cells to dLN, while blocking S1PR1 signaling led to an increased retention of CD4+ T cells in the kidney and a marked increase in tissue damage.


CD4+ T cells egress via the lymphatics out of the inflamed kidney is tuned by the downregulation of CXCR6 and upregulation of S1PR1. Blocking T cells egress leads to an increase in tissue damage, thus promoting the idea that T cell egress to the dLN alters organ-specific immunity.


  • Government Support – Non-U.S.