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Home » Infant T cells don’t remember pathogens–causes weaker immunity

Infant T cells don’t remember pathogens–causes weaker immunity

Last updated on December 4th, 2014 at 12:13 pm

active-immunityIf you hang out in various vaccine discussions, you will hear all kinds of odd, unscientific ideas about the immune system of infants. One of the major issues is a substantial oversimplification of the immune system (of adults and infants), mostly thinking it’s one “thing,” ignoring the complex physiology of the immune system which is an almost infinite number of interactions between cells, proteins and factors, organs, blood, fluids, and other physiological systems.

Generally, the popular assumption is that the infant immune system is weak, making those children more prone to viral or bacterial infections. The antivaccine crowd uses this belief to either state that vaccines won’t work or might actually harm the immune system, along with some overstated magical properties of human breast milk to prevent infection.

But according to a new study, led by Dr. Brian Rudd of the Department of Microbiology and Immunology at Cornell University, published in the Journal of Immunology, the immune system of newborns and infants is actually stronger than an adult’s immune system. Unfortunately, it has a short “memory.”

Without going through all the complex mechanisms of the immune system, basically there are a group of cells, called memory T cells, a subset of T lymphocytes, that are the center of the immune response to infection. Basically, a memory T cell remembers any pathogen it encounters–and when it meets up with that pathogen again, it mounts a faster and better defense against that pathogen. This is how vaccines work. They induce the production of these memory T cells against a particular pathogen, without the infection (meaning unregulated growth of the bacteria or virus). Without the memory T cells, a “natural” infection from a viral or bacterial pathogen can replicate so fast in a victim, that it could harm or even kill the individual before the T cells can mount an effective response.

Creating memory T cells in advance, through immunization, allows the immune system to mount a robust defense before the disease can gain a foothold and harm the victim. Once someone is vaccinated against a disease, the memory T cells do their job without the individual even noticing anything is going on. And that’s how the immune system works with vaccines. Interestingly, nearly 10% of the millions of T lymphocytes in adult humans are in a pool of memory cells, ready to engage the enemy pathogen if it shows up. The immune system is one incredibly beautiful network that keeps us alive.


During the first few months of an infant’s life, it is well understood that their immune system is not as capable of effectively fighting an infection as does the adult immune system. Dr. Rudd’s research showed that infants produced T cells that had a stronger and faster response to infection than adults. Unfortunately, those infant T cells did not end up in the memory pool of T lymphocytes like they do in adults. Thus, when an infant encounters the pathogen again, and because they have the more mature T cells, without the original memory, it can no longer respond to the pathogen as quickly as an individual who does have the pool of memory T cells–an infection then takes a higher toll.

So if an infant encounters a disease in early life, the pathogen isn’t “remembered”, so the immune system is required to restart the learning process when it encounters the same pathogen later in life. This is problematic for vaccinations, since they are dependent on the formation of memory T cells–but it can help build a vaccine development pathway that will eventually give us more powerful and longer-lasting vaccines.

According to Dr. Rudd, “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.”

Moreover, he added that the research group may be able to explore methods that induce the infant T cells to work more like adult memory T cells, so that they can “learn” from the vaccines earlier in life, and mount a better response to infections over time.

Interestingly, the teams found that the adult immune system did not produce protective cytokines, a hugely complex group of small proteins that signal various parts of the immune system and are important in the immune response. However, infant lymphocytes seems to produce these cytokines, which boosts the immune system against infection, though without any memory.

There are some issues with this study:

  • It’s in mice, and more than that, mice lymphocytes in cell culture. Though the results seem to support our observations about the human infant immune system, especially that it is weaker than the adult, it’s still mice.
  • Some of the observed responses seem to be small with large errors. Further experiments may help confirm what was shown.
  • The study doesn’t tell us why there’s this major difference, important information for those who develop vaccines going forward.
  • We don’t know when the infant T cells become more adult like. I assume it is over a range of time, but when?
  • Also, as far as I could tell, the authors didn’t examine the B memory cell response, which may or may not have the same issues. The B memory cells produce the antibodies that signal the T memory cells, both are required for an adequate memory response of the immune system.

The authors concluded that:

In summary, the data presented in this study provide new insight into impaired development of memory CD8+ T cells in early life. Our findings that neonatal CD8+ T cells skew toward a short-lived effector phenotype in a cell-intrinsic manner will need to be taken into account in the development of future strategies to enhance cellular immunity during early stages of development.

Since I can speculate more than an article in a peer-reviewed journal, I think there are several other things I can conclude:

  • Early infections in babies do not induce the adaptive immune memory, which helps the immune system defend itself against future pathogens. So those pox parties, where antivaccination parents intentionally expose to pathogens, are basically worthless. And immoral.
  • More evidence that protecting the baby by the herd effect is important. Because infants have an immature immune system, that won’t “remember” the infection, it’s important to keep those pathogens from attacking in the first place.
  • Early vaccinations may depend on other types of adaptive immune responses, including the B memory cells. However, we know that we can await the full “memory” of the immune system by waiting to administer some vaccines until several weeks or months after birth. Moreover, this makes boosters ever more critical. Those who push “revised vaccination schedules” are missing this point, that as the child’s immune system develops, it needs to have booster immunizations to build a larger supply of memory T cells. No, breast milk, vitamins, kale, sunshine, or organic foods are not going to induce these memory T cells, they ONLY form in response to the pathogen–either safely from a vaccination, or dangerously by catching the disease.
  • Finally, with this information in mind, vaccine development can be improved to the point where we can fine tune the vaccine to maximize the memory T cell response.

I like this kind of science. We observe something, that infants seem to not have a strong immune response to a disease, and scientists develop experiments to test hypotheses about that difference. And now we know more than we did a few months ago, which gives us critical information in preventing diseases with vaccinations.


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