New research by the University of Arizona Health Sciences has found a way by which infection affects the immune system that could lead to new immunotherapies to prevent disease and strengthen the ageing immune system.
The study has been published in the 'Nature Communications Journal'.
The immune system uses T cells, white blood cells that defend against pathogens such as viruses, bacteria and parasites, to fight infection. Prior research by Janko Nikolich-Zugich, MD, PhD, professor and head of the UArizona College of Medicine - Tucson's Department of Immunobiology, found that both the number and function of naive T cells - those that have never responded to an infection before - were negatively affected by ageing.
"The main population of cells that we lose in the process of ageing are naive T cells," Dr Nikolich-Zugich said.
"This study showed that both the maintenance of naive T cells over time and their function were improved by the presence of an infection, which aligns somewhat with the hygiene hypothesis that basically says if you allow your kids to be exposed to everyday germs, it's going to be better for them," Zugich added.
Previously, it was thought infections primarily affected the creation of memory T cells. When exposed to a pathogen, some naive T cells learnt and remembered, becoming memory T cells that prevented re-infection when they encountered the same pathogen again.
The recent UArizona Health Sciences study found a mechanism by which infection had the potential to strengthen the immune system against not only future attacks by the same pathogen but against different ones as well.
One of the ways the body regulated cell growth is through interleukins, naturally occurring proteins that mediate communication between cells. Interleukin 7 (IL-7), specifically, played an important role in naive T cell development and maintenance.
When the body detected a foreign invader, naive T cells were put into action by major histocompatibility complex (MHC) molecules, a group of genes on the surface of cells. MHC molecules took a portion of the pathogen and displayed it on the cell surface for recognition by the appropriate T cells. But in the absence of infection, MHC molecules also provided subtle "tickling" signals to naive T cells to keep them alive and able to receive IL-7 signals that kept their metabolism optimally tuned. The infected cells also secreted interferon type 1 molecules, which signalled additional immune responses.
"Now we know that when you have these fairly substantial infections, interferon type 1 molecules are making the MHC and Interleukin 7 signals stronger, more abundant and more available to naive T cells. It has never been shown that infection can do something like this," Dr Nikolich-Zugich said.
"This study showed that an infection not only better maintained the number of naive T cells, but it put them on a slightly higher state of alertness," Zugich added.
That meant when the immune system encountered a new infection, such as SARS-CoV-2 or a new strain of influenza, naive T cells would be able to respond faster and provide better protection.
Moving forward, Dr Nikolich-Zugich hoped to be able to determine how long the infection-mediated naive T cell response lasted, and if that depended on the presence of multiple or persistent infections.
Eventually, the UArizona Health Sciences research team wants to develop therapies that boost the immune system to fight disease by using naive T cells that are in a heightened state of alertness, to target things like cancerous tumours. They also hope to examine the feasibility of using the mechanism that maintains naive T cell production to strengthen the ageing immune system.
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