Researchers find a new way to halt age-related decline in immune system

Stanford University School of Medicine scientists have found that blocking the action of a single protein whose levels in our immune cells creep steadily upward with age can restore those cells’ response to a vaccine.

This discovery holds important long-term therapeutic ramifications, said Jorg Goronzy, MD, PhD, professor of rheumatology and immunology and the senior author of a study.

It might someday be possible, he said, to pharmacologically counter aging’s effects on our immune systems.

In the study, the Stanford team fingered a protein called DUSP6 that interferes with the capacity of an important class of immune cells to respond to the presence of a foreign substance, such as those appearing on the surface of an invading pathogen or in a vaccine designed to stifle that invasion.

The researchers also identified a potential lead compound that, by inhibiting DUSP6’s action, restores those cells’ responsiveness to a more youthful state.

A person’s immune response declines slowly but surely starting at around age 40, said Goronzy.

“While 90 percent of young adults respond to most vaccines, after age 60 that response rate is down to around 40-45 percent. With some vaccines, it’s as low as 20 percent,” he stated.

Vaccine failure among seniors poses a serious health problem: Some 90 percent of influenza deaths are among people over age 65.

“We are still far from application in the clinic. We need to keep tweaking the compound and testing it in mice to make absolutely sure it’s safe enough to try in humans,” cautioned Goronzy.

“But improving vaccine responses to overcome age-related immune defects represents a unique opportunity to attain healthy aging,” he added.

The new study will be published online in Nature Medicine. (ANI)

References:
Decline in miR-181a expression with age impairs T cell receptor sensitivity by increasing DUSP6 activity, Nature Medicine (2012) doi:10.1038/nm.2963