Immune Cells Share Information Like Bees
When bees come across new information, such as a good new source of honey, they share the news with other bees when they get back to the hive. Now new research from the US suggests the T cells of the immune system behave in a similar way when coordinating responses to disease pathogens and vaccines.
Scientists from the University of California - San Francisco (UCSF) write about their discovery in the 10 March online issue of Nature Immunology.
Senior author Matthew Krummel, is a professor of pathology at UCSF. He says in a statement that while the T cells don't do a dance to their co-cells in the same as bees do to fellow bees when they have news to share, they do gather together and share essential information in a similar way.
"They cluster together for the purpose of sharing information, transmitting what they've discovered about the new pathogen or vaccine, which in turn helps the immune system mount a coordinated response to the foreign matter," he explains, adding that the discovery could help development of new treatments to fight disease.
The discovery could be of particular interest to vaccine development, because this is an area of medicine that is still somewhat in the dark in trying to understand exactly how vaccines work.
"We know that they [vaccines] are effective for years after a vaccination, but we don't know why. It seems that T-cell aggregation is a profound part of the reason," says Krummel.
He and his colleagues found that after individual T cells have visited lymph notes and sampled foreign material such as vaccines, viruses and bacteria, they congregate for a while, several hours to one day after being exposed to the foreign material. Krummel and colleagues call this the "critical differentiation period".
The researchers suggest these "critical differentiation periods" are necessary to allow a "memory pool" to form in the immune system. It is access to this memory pool that enables the immune system to recognize pathogens it has been exposed to even years before.
If the immune system didn't have that long-term memory, vaccines would be useless, says Krummel.
"The body wouldn't remember that it had been exposed to a particular pathogen, such as measles or diphtheria, and would not know how to successfully fight it off," he adds.
For their study he and his colleagues worked with two sets of mice that were engineered to have a human-like immune system.
They vaccinated the mice against listeria, a bacterium that causes food poisoning, and then exposed the animals to the bacterium.
In one set of mice their immune systems were allowed to have normal critical differentiation periods, but in the other set of mice the researchers blocked the critical differentiation period.
The mice whose immune systems had normal, unimpeded critical differentiation periods, remained healthy and did not become infected.
The mice whose immune systems were blocked from having critical differentiation periods, fell prey to the infection, as if they had not been vaccinated at all, says Krummel.
Krummel's lab is currently trying to find new areas to investigate in immunology. He is excited by their new finding because it shows there is a "nexus" at which the T cells are bringing their responses together.
This means it may be possible to design cells to join that nexus, and do things we want them to do, he adds, for instance "push immune response in a particular direction, or enhance it overall".
Another way the finding could be useful is in the case of autoimmune diseases, such as lupus or diabetes. In such diseases the immune system is overactive. Blocking the formation of the memory pool could perhaps reduce the overactivity.
"You can't eliminate insulin, which is what much of the immune response is reacting to in diabetes," Krummel explains.
"But if you can tweak the immune cells in the right way, then although each cell would be responding to insulin, they would not be reacting as a group and thus may not become effective at killing the insulin-producing cells. That would severely weaken the autoimmune effect," he suggests.
However, although using mice adapted with human immune systems is a robust model for lab work, it will be years before the same kind of research can be done and proven in humans, says Krummel.
"We'll have to see what happens," he muses.
In a recent issue of Molecular Therapy, scientists from Stanford University School of Medicine describe how they developed a way to genetically engineer HIV-resistant cells, a method which if proven effective in humans, could give HIV-positive patients an alternative to the lifelong medication schedule that current patients now face.
Funds from the National Institutes of Health helped pay for the Krummel study.