Researchers identify cell group key to Lyme disease...( In an earlier study published in Na...),Health

In an earlier study published in Nature Immunology, Kronenberg, Sellati and co-workers had shown that a glycolipid, a type of fat, found in the membrane of Borrelia burgdorferi triggered an immune response from the NK T cells. "We had found that if you gave that lipid to mice or humans, it would activate NK T cells," Kronenberg said. While this suggested the cells might play a significant role in Lyme disease, "we were missing in vivo (in the body) evidence showing that the NK T cells were activated following infection and were important for killing and clearing the Lyme disease bacteria," he said, noting that the latest study demonstrates this in an animal model.

Sellati said the finding is particularly important because it opens new lines of investigation as to the causes of chronic Lyme disease. "That's what's so exciting when you identify a new cell type as playing a central role in preventing the disease process," he said. "So in those individuals who have a more severe form of the disease, you can study their NK T cells and see if there's some deficiency that prevents those NK T cells from killing and clearing the bacteria."

In their studies, the researchers worked to model the natural route of Lyme disease infection as closely as possible. "The way people typically get Lyme disease is that they're out hiking and they get bitten by a deer tick," said Kronenberg. "So what we did in the lab was to get ticks infected with Borrelia burgdorferi from collaborators at the University of Connecticut Health Science Center and then used those ticks to infect mice in a confined and controlled environment."

The researchers used one group of mice genetically engineered not to have NK T cells, while the control group had the cells. "The mice that didn't have NK T cells were not as capable of clearing the (Lyme disease) bacteria," Kronenberg said. "And they developed a chronic arthritis, while the control mice did not." He s
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