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A new tool against brain disease

ssion, the higher the patient's viral load and the lower the count of helper T cells, said Walker.

When they compared PD-1 activation in blood samples from four patients before and after antiviral therapy, they found that PD-1 expression dropped when treatment began. "It became very clear from this analysis that the virus was actually driving these high levels of PD-1 expression, and that you could actually change the PD-1 level by getting rid of the viral antigen with drugs," said Walker. An antigen is a protein on a virus or other infectious agent that triggers an immune reaction.

Walker said one of the team's key findings emerged from their test tube studies showing that blocking the PD-1 pathway could restore the function of exhausted killer T cells. "We wanted to determine whether these T cells had been irreparably damaged or misprogrammed," he said. "And we found that they are capable of functioning; they've just been turned off."

Similarly, the researchers also found that blocking PD-1 restored helper T cell function. "This was the most striking finding, because the majority of patients we have studied had no detectable levels of these HIV-specific cells; but as soon as we blocked the PD-1 pathway, they had a ton of them," said Walker.

The researchers' discoveries could lead to immediate clinical application, although Walker cautioned against over-optimism. "Obviously, the big question is whether you could manipulate this pathway in HIV-infected people to turn these T cells back on and better control the virus," he said. "And drugs to block this pathway have already been developed for cancer, so that question should be able to be addressed in the very near future.

"However, one has to proceed with real caution, because if you turn back on an immune regulatory switch that the body has decided to turn off, you could trigger serious immunological problems such as
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Source:leesiegel@ucomm.utah.edu


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