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Study suggests way to re-energize immune response to chronic viral infection

Like boxers wearied by a 15-round bout, the immune system's CD8 T cells eventually become "exhausted" in their battle against persistent viral infection, and less effective in fighting the disease.

In a study to be published Dec. 28 on the journal Nature's website, researchers at Dana-Farber Cancer Institute and Emory University have traced the problem to a gene that turns off the infection-fighting drive of CD8 T cells in mice. The discovery raises the possibility that CD8 cell exhaustion can be reversed in human patients, reinvigorating the immune system's defenses against chronic viral infections ranging from hepatitis to HIV, the virus that causes AIDS.

"CD8 T cells that have fought viral infections retain a 'memory' of the viruses they've encountered, so they can rapidly respond to new infections from those viruses," says the study's author, Gordon Freeman, PhD, of Dana-Farber. In the case of chronic infection, however, senior author Rafi Ahmed, PhD, of Emory, has shown that memory cells become exhausted and lose the capacity to respond to the virus. Why this occurs, on a molecular level, has been unclear.

To find the cause, Freeman and his colleagues conducted a "microarray" experiment measuring the activity of thousands of genes in normal memory CD8 T cells in mice and in "exhausted" versions of those cells. They found that a gene known as PD-1 was much more active in the exhausted cells.

From previous research, Freeman's team knew that PD-1 is responsible for a specialized "receptor" in CD8 cells -- a tiny socket for receiving signals from other cells. In 2001, Freeman and his colleagues showed that when the PD-1 receptor latches onto a molecule called PD-L1, the immune system's response to infection is weakened. Freeman's team made antibodies to block this interaction.

"When [co-author] John Wherry of the Wistar Institute found a high level of the PD-1 gene in microarray experiments, we wanted to test whether thi
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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
28-Dec-2005


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