How T Cells Form Memories of Viruses

A new scientific research has revealed another hidden ability our immune systems have. The work evidenced the mechanism employed by our body's natural defense mechanism in “learning” the identity of a pathogen, a feature that allows immune cells to respond faster and more effective the next time around. According to the investigation, the effect occurs even in the first days after a major viral infection, which is a lot faster than originally thought, PhysOrg reports.

When a virus invades, white blood cells known as T cells are in charge with an immediate response. Of these immune cells, the vast majority attack the invader head-on, consuming and destroying it, and dying themselves in the process. Still, a very small portion of these effector cells manage to survive, and differentiate into something else – a new type of cells called memory T cells. These are the main factors that promote an immune response the next time the same viral agent enters the body. What researchers managed to identify in the new study was the molecular mechanism that promoted this different type of differentiation – as in which of the T cells became a memory cell, and which turned into an attacker.

The finding is extremely important, because it could hold hints on creating future vaccines or therapy approaches for conditions such as HIV/AIDS, or even select types of cancer. Details of this amazing work appear in this week's issue of the scientific journal Immunity. The study was authored by the Director of the Emory Vaccine Center, Rafi Ahmed, PhD. The expert is well known for his work in this field of research, and is also a Georgia Research Alliance Eminent Scholar, as well as a member of the National Academy of Sciences.

Working together with a number of postdoctoral fellows at the Emory University, the expert was able to determine that the molecule CD25 was directly involved in T-cell differentiation. This molecule is very important, because it promotes immune-cell sensitivity to interleukin 2 (IL2), a growth factor that stimulates the development of T cells. “Apparently, cells that receive prolonged IL-2 signals are pushed further down the effector path and hence exhibit decreased potential to form long-lived memory cell. It may be beneficial that not all of the T cells burn themselves out fighting the virus so that memory-fated cells can conserve resources for the next encounter,” postdoctoral fellow Surojit Sarkar says.