Anytime a new bug comes around, experts warn that those most susceptible to the germs are generally the elderly and infants. But a new study from Cornell University has found that infant’s immune systems are actually rather strong. However, the immunities that infant’s bodies create often don’t last too long.
For the longest time, experts believed that weak immune cells were the culprit in babies being vulnerable to infections. However, they now believe that it is “forgetful” immune cells, rather than the cells being weak. The study found that in mice, an infant’s immune system was quick to respond to an infection. In fact, it responded with more strength and speed than adults. However, these immunities that were created did not last.
The research study was published in the Journal of Immunology earlier this month. The groundbreaking findings suggest that a better approach to immunizations can be taken in order to protect babies and children from infectious diseases, which account for more than one-third of infant deaths across the world, according to the World Health Organization. Immunizations and vaccines work to protect our bodies by “teaching” our immune systems to keep pathogens stored in their memory. However, when an infant is immunized, their immunities rapidly decrease, often requiring them to need an extra set of booster shots after their initial immunizations.
The study’s lead author, Brian Rudd, from the College of Veterinary Medicine says,
“The perfect vaccine would be a single dose given at birth that generates long-lasting immunity. No such vaccine exists because we haven’t understood why infants rapidly lose immunities. Our finding could change the way we immunize infants and ultimately lead to more effective ways of enhancing immunity in early life.”
To be immune to most microbes depends on T cells that remember the specific pathogens, which can respond quickly to future infections. Adults’ immune systems typically always create large numbers of these “memory T cells” during an infection. Approximately ten percent of them stay within a long-lasting “memory pool,” which stay there in order to respond quickly to an infection the next time. During the study, Rudd discovered that newborn T cells that were created in response to infection turned out very differently. When put together with the same pathogen, newborn immune systems in the mice made T cells that had responded quicker to infection than adult cells typically do, but rapidly decrease, thus never making it to the long-living “memory pool.”
Rudd says “Surprisingly, we found that newborns’ cells actually responded more vigorously to infection compared to adults. We also found that newborns’ cells go through their lifespans more quickly and die off sooner, before they can give rise to memory T cells and remember what they’ve learned. So the immune system is forced to start the learning process over again when infected by the same pathogen later in life.” He is also exploring how different proteins in various-aged T cells determine how a developmental variation in the factors might influence the “memory cells” behavior and ultimate fate.
He also says,
“We hope to find a way to make neonatal cells behave more like adult cells in how they learn from vaccines and respond to infection. Knowledge gained from these studies could be used to design more effective therapeutic interventions and vaccines that can be safely administered in early life.”
Rudd’s project was funded and supported by the Cornell Center for Vertebrate Genomics, National Institutes of Health and a National Science Foundation Graduate Research Fellowship.