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Way to Rescue Tired Immune Cells Fighting HIV Found
Date:11/12/2008

Discovery of pathway could lead to new treatments, researchers say

WEDNESDAY, Nov. 12 (HealthDay News) -- A method of "rescuing" immune cells exhausted from fighting HIV infection has been discovered by American and Canadian researchers.

They found that a molecule called Tim-3 is present at high levels in poorly functioning immune cells worn out from combating HIV, the virus that causes AIDS. Blocking the activity of Tim-3 improved the function of these cells, so that they could jump back into the fight against HIV infection, said the University of California, San Francisco (UCSF), and University of Toronto researchers.

"In the typical course of HIV infection, an initial burst of very high levels of the HIV virus is brought partially under control by the infected person's immune system, specifically by an immune system cell called a CD8+ killer T-cell. In the majority of cases without antiretroviral drug treatment, the immune system is eventually overwhelmed, and progression to AIDS occurs," co-principal author Brad Jones, a doctoral candidate in immunology at the University of Toronto, said in a news release about the study.

In a group of HIV-infected patients, the researchers observed that Tim-3 expression on CD8+ T-cells was associated with clinical parameters of HIV disease progression. This led them to believe that manipulation of the Tim-3 pathway may provide a new approach to HIV treatment.

To test their theory, they developed a molecule that blocks the Tim-3 signal and studied its effect on CD8+ T-cells in the laboratory. They found that blocking the Tim-3 pathway rescued the immune cells and restored their ability to fight infection.

The study was expected to be published in the Nov. 24 issue of the Journal of Experimental Medicine.

"We still do not know how the virus triggers Tim-3 or if this is restricted to HIV infection, but our findings may provide a new direction to vaccines and therapies that will potentially reverse these dysfunctional cells and allow them to control HIV-1 replication," co-principal author Lishomwa Ndhlovu, of the division of experimental medicine at UCSF, said in the news release.

"Our hope is this will enable those infected with HIV to turn the tide in the long battle between the immune system and HIV. Future studies which block Tim-3 signaling in animal models of chronic viral infection will help to evaluate the therapeutic potential of this approach," Jones added.

More information

The U.S. National Institute of Allergy and Infectious Diseases has more about HIV/AIDS.



-- Robert Preidt



SOURCE: University of California, San Francisco, news release, Nov. 10, 2008


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