Interleukin-15 is a major regulator of the cell-microenvironment interactions in human renal homeostasis. Giron-Michel, J., Azzi, S., Ferrini, S., Chouaib, S., Camussi, G., Eid, P., & Azzarone, B. Cytokine Growth Factor Rev, 24(1):13–22, February, 2013. ![Interleukin-15 is a major regulator of the cell-microenvironment interactions in human renal homeostasis [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper abstract bibtex Experiments in IL-15(-/-) and IL-15Ralpha(-/-) mice show that intra-renal IL-15, through IL-15Ralpha behaves as an epithelial survival factor. Recent data highlight new functions of IL-15 in renal homeostasis mediated by IL-15Rgamma (CD132). Indeed, in CD132+ renal epithelial tubular cells IL-15 preserves E-cadherin expression inhibiting epithelial-mesenchymal transition (EMT). By contrast, during allograft rejection, the increased intra-graft IL-15 expression favors tubular destruction facilitating the intraepithelial recruitment of CD8 T cells expressing the E-cadherin ligand CD103. In renal cancer, loss of CD132 by epithelial cells defines a tumoral microenvironment where IL-15 triggers E-cadherin down-regulation and EMT. Finally, in CD132+ renal cancer stem cells IL-15 induces the generation of non-tumorigenic epithelial cells sensitive to cytotoxic drugs. These findings are discussed in the light of IL-15-based immunotherapy for renal cancer.
@article{giron-michel_interleukin-15_2013,
title = {Interleukin-15 is a major regulator of the cell-microenvironment interactions in human renal homeostasis},
volume = {24},
issn = {1879-0305 (ELECTRONIC) 1359-6101 (LINKING)},
shorttitle = {Interleukin-15 is a major regulator of the cell-microenvironment interactions in human renal homeostasis},
url = {http://www.ncbi.nlm.nih.gov/pubmed/22981349},
abstract = {Experiments in IL-15(-/-) and IL-15Ralpha(-/-) mice show that intra-renal IL-15, through IL-15Ralpha behaves as an epithelial survival factor. Recent data highlight new functions of IL-15 in renal homeostasis mediated by IL-15Rgamma (CD132). Indeed, in CD132+ renal epithelial tubular cells IL-15 preserves E-cadherin expression inhibiting epithelial-mesenchymal transition (EMT). By contrast, during allograft rejection, the increased intra-graft IL-15 expression favors tubular destruction facilitating the intraepithelial recruitment of CD8 T cells expressing the E-cadherin ligand CD103. In renal cancer, loss of CD132 by epithelial cells defines a tumoral microenvironment where IL-15 triggers E-cadherin down-regulation and EMT. Finally, in CD132+ renal cancer stem cells IL-15 induces the generation of non-tumorigenic epithelial cells sensitive to cytotoxic drugs. These findings are discussed in the light of IL-15-based immunotherapy for renal cancer.},
number = {1},
journal = {Cytokine Growth Factor Rev},
author = {Giron-Michel, J. and Azzi, S. and Ferrini, S. and Chouaib, S. and Camussi, G. and Eid, P. and Azzarone, B.},
month = feb,
year = {2013},
pages = {13--22},
}
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