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MIP‐3α/CCL20 in Renal Transplantation and Its Possible Involvement as Dendritic Cell Chemoattractant in Allograft Rejection
Author(s) -
Woltman Andrea M.,
De Fijter Johan W.,
Van Der Kooij Sandra W.,
Jie Kim E.,
Massacrier Catherine,
Caux Christophe,
Daha Mohamed R.,
Van Kooten Cees
Publication year - 2005
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2005.00997.x
Subject(s) - medicine , transplantation , chemotaxis , ccl20 , dendritic cell , immunology , chemokine , immune system , receptor , chemokine receptor
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.