pped blood flow to kidneys in mice in both groups for 30 minutes, they discovered that the kidneys in the injected mice were improved compared to the other group of mice.

This was an unexpected result, says Rabb. For years we have known that T cells play a role in IRI, but we assumed it was always a negative role; now we know they play a protective role as well.

Rabb said further research is needed to establish the exact mechanism for this protection, but he says it makes perfect sense in theory.

T cells are part of our immune system, and our immune system is designed to protect us from injury. Whats surprising here is that practical experience over the years has taught us that when the immune system is activated, we have increased cell damage, says Rabb.

Using a new method developed by Dolores B. Ascon, Ph.D., a postdoctoral fellow in the Department of Nephrology at Hopkins and first author on the paper, Rabb and his team successfully tracked small numbers of lymphocytes in three distinct groups of mice: normal mice, mice that underwent fake surgery without blood flow interruption to the kidneys (ischemia) and mice that underwent surgery and 30 minutes of ischemia.

The study showed elevated levels of T cells in the kidneys three hours after IRI compared to the normal mice. It also showed elevated levels of the chemicals tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma), which are known to produce cellular damage in kidneys. These chemicals are produced by T cells.

The mice that underwent fake surgery also had an elevated level of T cells when compared to the normal mice, but these cells did not release TNF-alpha and IFN-gamma and did not cause injury to the kidneys.

In this case it appears as though the surgery triggered the movement of T cells to the region, but since there was no ischemia, these cells did not produce TNF-alpha and IFN-gamma, says Rabb. This
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