| First Author | Wang S | Year | 2008 |
| Journal | Kidney Int | Volume | 73 |
| Issue | 3 | Pages | 318-26 |
| PubMed ID | 18004294 | Mgi Jnum | J:152883 |
| Mgi Id | MGI:4360172 | Doi | 10.1038/sj.ki.5002692 |
| Citation | Wang S, et al. (2008) Decreased renal ischemia-reperfusion injury by IL-16 inactivation. Kidney Int 73(3):318-26 |
| abstractText | T-cell-mediated renal injury is a major cause of kidney transplant rejection and renal failure; hence, understanding T-cell migration within the kidney is important for preventing renal injury. Interleukin (IL)-16 is a T-cell chemoattractant produced by leukocytes. Here we measured IL-16 expression in the kidney and its role in renal ischemia-reperfusion injury induced by different conditions in several strains of mice. IL-16 was strongly expressed in distal and proximal straight tubules of the kidney. The IL-16 precursor protein was cleaved to a chemotactic form in cultured tubular epithelial cells. Inactivation of IL-16 by antibody therapy or IL-16 deficiency prevented ischemia-reperfusion injury as shown by reduced levels of serum creatinine or blood urea nitrogen compared to control mice. Further studies indicated that fewer CD4-cells infiltrated the post-ischemic kidneys of IL-16-deficient mice and that the protective effect of IL-16 antibody treatment was lymphocyte-dependent. Our results suggest that IL-16 is a critical factor in the development of inflammation-mediated renal injury and may be a therapeutic target for prevention of ischemia-reperfusion injury of the kidney. |
