DURHAM, N.C. An immune system response that is critical to the first stages of fighting off viruses and harmful bacteria comes from an entirely different direction than most scientists had thought, according to a finding by researchers at the Duke University Medical Center.
"This finding will have important implications in vaccine science and autoimmune disease therapy development," said Michael Gunn, M.D., an immunologist and cardiologist at Duke and senior author of the study published in Nature Immunology.
Type 1 helper (TH1) T cell immune responses are critical for the control of viruses and certain bacteria. Immunologists have generally believed that TH1 responses are induced by rare immune cells, called dendritic cells. When activated by infection or vaccination, the dendritic cells were thought to move from peripheral tissues into lymph nodes to stimulate T cell responses.
The Duke researchers found, however, that the dendritic cells that stimulate TH1 responses didn't come from peripheral tissues, but rather arose from monocytes, a common cell type in the blood, that moved directly into lymph nodes after infection.
"The result speaks to the most basic principles of immune response to pathogens," Gunn said. "It may also explain the poor results we have seen in attempts to develop effective dendritic-cell vaccines."
Gunn previously had identified a particular protein, known as a chemokine, that stimulates the migration of activated dendritic cells from peripheral tissues to lymph nodes. The Duke researchers generated a TH1 response in laboratory mice that lacked this chemokine with influenza viruses.
"We really thought the mice would not be able to generate much of an immune response at all," Gunn said, because they wouldn't be able to mobilize dendritic cells. "The mice, however, had increased TH1 responses. We knew we had to find what was really causing the response."
|Contact: Mary Jane Gore|
Duke University Medical Center