"Our findings were unexpected," says Dale Umetsu, MD, PhD, an
immunologist at Children's Hospital Boston and senior
investigator on both the human and mouse studies. "They suggest
we need to look at asthma in a different way in terms of
therapies." Asthma affects 20 million people in the U.S., and in
2003 caused nearly 2 million emergency-department visits.
Previously, scientists believed that conventional CD4+ T
lymphocytes – specifically, type 2 helper cells (Th2 cells) –
were causing the inflammatory process that is central in the
disease. Corticosteroids, the current mainstay of asthma
therapy, target Th2 cells, along with other inflammatory cells.
But in 2003, Umetsu and co-investigator Omid Akbari, PhD, both
then at Stanford University, showed in Nature Medicine that
activation of NKT cells is required for the development of
asthma in mice: Mice that lacked NKT cells did not develop
airway hyperreactivity, a cardinal feature of asthma. And this
year, in the February 21 Proceedings of the National Academ