MIP-3α/CCL20 in renal transplantation and its possible involvement as dendritic cell chemoattractant in allograft rejection

Andrea M. Woltman*, Johan W. De Fijter, Sandra W. Van Der Kooij, Kim E. Jie, Catherine Massacrier, Christophe Caux, Mohamed R. Daha, Cees Van Kooten

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

34 Citations (Scopus)

Abstract

Graft-infiltrating dendritic cells (DC) and alloreactive T lymphocytes play a critical role in renal allograft rejection. Renal proximal tubular epithelial cells (TEC) are considered as active players in the attraction of leukocytes during renal inflammatory responses. Macrophage inflammatory protein (MIP)-3α/CCL20 is a major chemokine expressed by epithelial cells that attracts immature DC. In the present study, we present evidence that also the transplanted kidney can be a major source of MIP-3α/CCL20. Renal transplant recipients with rejection showed significantly increased excretion of urinary MIP-3α/CCL20 that correlated with transplant function. The tubular staining for MIP-3α/CCL20 in renal biopsies of patients with rejection as well as in vitro studies with primary human TEC indicated that TEC might be responsible for the increased urinary MIP-3α/CCL20. Furthermore, MIP-3α/CCL20 produced by activated TEC was highly potent in the attraction of CD1a+CD34+-derived DC precursors. These data suggest a role for MIP-3α /CCL20 in amplification of the immune response during renal allograft rejection by attraction of CCR6+ inflammatory cells, which may include DC, to the site of inflammation.

Original languageEnglish
Pages (from-to)2114-2125
Number of pages12
JournalAmerican Journal of Transplantation
Volume5
Issue number9
DOIs
Publication statusPublished - Sept 2005
Externally publishedYes

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