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Prior studies have shown that the DNA damage pathway is activated in precancerous lesions, as well as many advanced tumors. In addition, many cancer cells express Rae1. It has been known that when genetic abnormalities occur, the cell cycle is halted so that the cell has time to fix the damage before the DNA is replicated. If the damage is too severe for the cell to repair on its own, it can trigger cell death, a process known as apoptosis.

"All of this is happening autonomously within the cell," said Raulet. "What's new about our study is that we found that cells with damaged DNA can also involve other cells in the fight, triggering a mechanism that signals other cells - specifically NK cells - to attack. It could be another ingenious trick that the body uses to ward off cancerous cells."

Interestingly, the NKG2D receptor is also found on the CD8+ T cell, a type of immune cell that acts as a sentry with a long-term memory of prior invaders. These cells stand ready to find and destroy cells infected by viruses before the virus can spread.

"We don't have direct information about the role of the DNA damage pathway in regulating immune responses to infectious diseases, but given what we have shown here, it is certainly plausible that it contributes to the expression of the NKG2D ligand," said Raulet. "It may also be that the Rae1 ligand helps trigger T cell responses that contribute to long term specific immunity. It's certainly an area of research that warrants more study."

Other co-authors of the paper are Sandra Orsulic, assistant professor at the Massachusetts General Hospital Center for Cancer Research, and Eric Brown, assistant professor at the University of Pennsylvania School of Medi
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Source:University of Bristol