TY - JOUR
T1 - MIP-3α/CCL20 in renal transplantation and its possible involvement as dendritic cell chemoattractant in allograft rejection
AU - Woltman, Andrea M.
AU - De Fijter, Johan W.
AU - Van Der Kooij, Sandra W.
AU - Jie, Kim E.
AU - Massacrier, Catherine
AU - Caux, Christophe
AU - Daha, Mohamed R.
AU - Van Kooten, Cees
PY - 2005/9
Y1 - 2005/9
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=27844595393&partnerID=8YFLogxK
U2 - 10.1111/j.1600-6143.2005.00997.x
DO - 10.1111/j.1600-6143.2005.00997.x
M3 - Article
C2 - 16095490
AN - SCOPUS:27844595393
SN - 1600-6135
VL - 5
SP - 2114
EP - 2125
JO - American Journal of Transplantation
JF - American Journal of Transplantation
IS - 9
ER -