The biological control of the immune system is perhaps the most neglected of all the biological processes.
It is also one of the most overlooked.
And the new study published in Molecular Psychiatry suggests that we are beginning to understand how that control is achieved.
“This study shows us how a single gene can alter the immune response in the context of a whole host of biological processes,” said lead author Maria Elena Vitti, a postdoctoral fellow at the Institute of Psychiatry and Biobehavioral Sciences in Naples, Italy.
“It’s a fascinating and important contribution.”
The study involved the identification of a gene, called GSK-3, that controls a protein called T-cells, which are part of the central nervous system.
These are cells that release the antibodies that fight off foreign invaders and keep them from invading the brain and other organs.
They also release a hormone called interleukin-6, which is known to cause inflammation and damage to the immune cells.
The T-cell-mediated signaling pathway is critical to how the immune systems attack and attack infection, and it also controls how a person’s body responds to various kinds of trauma.
“The T cells are like the ambulance of the body,” said Vitto.
“They help us control a number of other functions of the system.
It’s important for a person to know how to manage these T cells, so they can control the immune responses in the body.”
The researchers identified T- cells from patients who had received a severe brain injury.
“A lot of people don’t realize how the T cells actually do their work, and so it’s really important to study how the brain reacts to trauma,” said study co-author Raffaele Bonfante, a professor at the University of Trento in Italy.
The researchers found that in the brains of people who received a mild brain injury, the levels of T- and interleucin-4, a protein that helps regulate inflammation, rose significantly.
This was accompanied by a reduction in levels of interleuin-5, which acts as a stress-relieving hormone.
The researchers believe that T- or interleutin-3 may act as a trigger for T-cord inflammation, which they have found in other studies.
“In these studies, the T-Cell responses were clearly increased, whereas the interleusin-7 responses were not.
They were basically not different,” said Bonfanti.
The interleukemic effect, in turn, was accompanied in this case by a rise in T-Cord and interferon-α levels.
This is a signal that the body’s immune system has been activated, and therefore it’s very important to keep this balance, he added.
“In addition, the interferons are actually signaling T cells that are not working.
These T cells have been turned on and turned off, and this is exactly what happens in TBI.””
These interleukes were not produced in response to a single injury,” said Dr. Joachim Heidt, director of the Brain and Cognitive Imaging Laboratory at the Swiss Federal Institute of Technology in Lausanne.
“We had a lot of patients with different injuries, and there was no clear correlation between their responses and their responses in response in a previous study.
It was interesting that T cells from these patients had a different response to the TBI than those from other patients.””
The findings suggest that T cell activation in the brain may be a mechanism by which TBI can induce the inflammatory response in T cells,” said co-senior author Dr. Andreas Zettermann, director for Neurogenetics at the Federal Institute for Medical Research in Bern.
“But the mechanism is not clear.”
The next step is to look at how the interLEU-3 response changes as a result of exposure to stressors, and to look for potential triggers.
For example, a T cell that responds to a high level of interLEu-3 in response not only to stress but to stress itself, but also to infection could potentially be an additional trigger.
The research is described in the journal Molecular Psychiatry.