As we age, a variety of changes occur in our body. Some are very visible — wrinkles, graying hair — and some are almost impossible to see on the surface. It’s been known for a long time that the immune system takes a hit as we grow older, but it has been hard to pinpoint the underlying mechanisms of this process. Developing therapies or medications to preserve our immune systems is almost impossible without this background knowledge, so scientists from the Florida campus of Scripps Research Institute (TSRI) took a look at just how aging cripples the immune system.

The research, published in Cell, centers on an organ called the thymus, which produces T lymphocytes. These cells are critical to the immune system and must be constantly replenished to respond to new threats.

"The thymus begins to atrophy rapidly in very early adulthood, simultaneously losing its function," said TSRI Professor Howard Petrie, in a press release. "This new study shows for the first time a mechanism for the long-suspected connection between normal immune function and antioxidants."

Petrie and his team developed a computational method for analyzing the activity in two of the major thymic cells — stromal cells and lymphoid cells. They examined these cells in mouse tissues, which are similar to human tissues in terms of age-related atrophy and function. Researchers found a deficiency of an antioxidant enzyme called catalase in the stromal cells, which had resulted in high levels of reactive oxygen by-products of metabolism and, consequently, quicker metabolic damage.

In order to confirm the significant role of catalase, the researchers increased levels of the enzyme in animal models and found that it preserved the thalamus size for a much longer period. Also, animals that were given two common dietary antioxidants, including vitamin C, were protected from aging effects on the thalamus.

These findings in combination support the “free-radical-theory” of aging — a suggestion that reactive oxygen species produced during animal metabolism cause damage to cells that contributes to aging and age-related diseases.

Past studies have suggested that sex hormones, including androgens like testosterone, play an important role in the aging process. These studies, however, failed to answer a key question: Why does the thymus atrophy so much more quickly than other body tissues?

"There's no question that the thymus is remarkably responsive to androgens," Petrie said, "but our study shows that the fundamental mechanism of aging in the thymus, namely accumulated metabolic damage, is the same as in other body tissues. However, the process is accelerated in the thymus by a deficiency in the essential protective effects of catalase, which is found at higher levels in almost all other body tissues."

Source: Griffith A, et al. Metabolic Damage and Premature Thymus Aging Caused by Stromal Catalase Deficiency. Cell. 2014.