They are at the forefront in the fight against viruses, bacteria, and malignant cells: the T cells of our immune system. But the older we get, the fewer of them our body produces. Thus, how long we remain healthy also depends on how long the T cells survive. Researchers at the University of Basel have now uncovered a previously unknown signaling pathway essential for T cell viability.

Like human beings, every cell in our body tries to ward off death as long as it can. This is particular true for a specific type of immune cells, called T-lymphocytes, or T cells for short. These cells keep viruses, bacteria, parasites and cancerous cells at bay. While T cell production is an active process in infants, children and young adults, it comes to a gradual stop upon aging, meaning that in order to maintain adequate immunity up to an old age, your T cells should better live as long as you.

How T cells manage to survive for such a long time, up to several decades in humans, has long remained unclear. In collaboration with scientists at the Department of Biomedicine and sciCORE, the Center for Scientific Computing of the University of Basel, Professor Jean Pieters’ research group at the Biozentrum has now revealed the existence of a hitherto unrecognized pathway promoting long-term survival of T cells. In Science Signaling they report that this signaling pathway, regulated by the protein coronin 1, is responsible for suppressing T cell death.

An experimental vaccine successfully eliminated aging cells from the bodies of mice, helping to prolong the rodents’ lives and reverse some signs of age-related disease. The researchers say the experiment is a step on the road to a similar vaccine for humans, but could it really work?

More than a million Americans undergo knee and hip replacements each year. It’s a last resort treatment for pain and mobility issues associated with osteoarthritis, a progressive disease caused by degeneration of the protective layer of cartilage that stops our bones grinding together when we sit, stand, write, or move around.

But what if doctors could intervene and repair damaged cartilage before surgery is needed?

For the first time, researchers at the Keck School of Medicine of USC have used a stem cell-based bio-implant to repair cartilage and delay joint degeneration in a large animal model. The work will now advance into humans with support from a $6 million grant from the California Institute of Regenerative Medicine (CIRM).

Researchers say they have found a growth hormone in the colon that helps damage DNA, which aides in the aging process. The finding could lead to new therapeutic approaches to aging-associated disorders like cancer.

Whereas circulating pituitary growth hormones decline with age, non-pituitary growth hormones, or npGH, increase with age. That means the colon tissue growth hormone helps initiate the first stages of tumor development and influence the aging process, Cedars-Sinai Medical Center researchers said in research published in the journal Cell Reports.

At the core of the issue is npGH blocking a certain protein from protecting DNA from damage. The protein, p53, is a tumor suppressor that helps repair DNA, but it can also awaken growth hormones.