In an example of biological irony, the same white blood cell chemistry known to damage kidneys used for transplants may also help prevent such damage, according to a federally// funded study in genetically engineered mice at Johns Hopkins.
Researchers have long known that when blood flow is cut off and then returned to transplanted kidneys or other organs, immune system cells called T lymphocytes produce toxic natural chemicals that contribute to ischemic reperfusion injury (IRI). Nature cannot distinguish between deliberate surgical wounds needed to remove and re-implant a donor kidney and other kinds of organ damage in which certain toxic chemicals are needed to clean up or remove bad tissue.
But in the new study published in the September issue of The Journal of Immunology, the Hopkins team reports that that T cells can also play a role in reducing cellular damage in IRI kidneys, according to Hamid Rabb, M.D., medical director of kidney and pancreas transplantation at The Johns Hopkins University School of Medicine.
IRI occurs in 30 percent to 40 percent of kidneys removed from dead donors, resulting in lower kidney survival rates, shortened kidney life and a cost increase of approximately $20,000 per patient from the initial hospital stay and treatment alone, according to Rabb. Scientists therefore are interested in identifying means of preventing or rapidly treating IRI, but one barrier to greater understanding has been the inability to detect the lymphocytes in the kidney during the first critical six hours after blood flow is returned.
In the Hopkins study, designed to try to find these cells and learn more about IRI, white blood cells were taken from mice that had undergone experimentally induced IRI. These cells were injected into mice engineered without a thymus gland, which produces T cells. A comparison group of genetically engineered mice got no injections.
After the researchers temporarily sto
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