Th17 cells can promote inflammation that is important for protection against pathogens, but they have also been implicated in diseases like multiple sclerosis, psoriasis, rheumatoid arthritis, and ankylosing spondylitis. Treatment options for some of these diseases, such as psoriasis, include manipulating T cell function.
David Hafler's group at Yale University studies human autoimmune diseases in general and the role of Th17 cells in particular, and has collaborated with Kuchroo's group for many years. "These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment," said Hafler, Gilbert H. Glaser Professor of Neurology, professor of immunobiology, chair of Department of Neurology, and senior author of one of this week's Nature papers.
Some genes have been previously tied to Th17 development, but the research team wanted a more comprehensive view. One of the challenges of studying cell development, however, is that cells, particularly immune cells, change and evolve over time. The researchers chose to take frequent snapshots 18 over the course of three days to see what was happening within the T cells as they grew from nave cells into more specialized Th17 cells. From these snapshots, they used computational algorithms to begin to stitch together a network of molecular changes happening as the cells matured.
With this initial information in hand, the researchers systematically tested their model by silencing genes one-by-one, which could help reveal the most important points in the network and untangle their biological me
|Contact: Haley Bridger|
Broad Institute of MIT and Harvard