According to many of the researchers, the main contributors to multiple sclerosis are environmental and genetic factors. Researchers from the University Of Geneva (UNIGE) and the Geneva University Hospitals (HUG), Switzerland observed the mechanism of transient cerebral viral infections in the early stage of life and the progression of this autoimmune disease as the mouse model ages.
Infection in the brain in early childhood make such changes in the brain that triggers the immune system to work against it promoting autoimmune lesions. The findings of the research paper “Brain-resident memory T cells generated early in life predispose to autoimmune disease in mice” are published in the journal Science Translation Medicine.
Currently, there is no cure for multiple sclerosis. Researchers are unaware of the causes behind the development of disease at the age of 30.
Doron Merkler, lecturer in the sector of Pathology and Immunology in UNIGE’s Faculty of Medicine and a top counselor in the Clinical Pathology Service of the HUG said: “We asked ourselves whether brain viral infections that could be contracted in early childhood were among the possible causes.”
Normally the immune system starts its work quickly against these transient brain infections. The person stays unaware of this whole mechanism going on “But these transient infections may, under certain circumstances, leave a local footprint, an inflammatory signature, in the brain,” the scientist says.
In order to carry out the study, researchers triggered the transient viral infection in groups of both aged and young mice.
Karin Steinbach, a member of the research team adds, “In both cases, the mice showed no signs of the disease and eliminated the infection within a week with a similar anti-viral immune response.”
Both of the groups were left to become old before administrating self-reactive cells. These cells have the potential to disturb the healthy brain structure. It is also considered as a contributor to the severity of multiple sclerosis patients.
Karin Steinbach says, “In both cases, the mice showed no signs of the disease and eliminated the infection within a week with a similar anti-viral immune response.”
The self-reactive cells were not able to make their journey to the brain in elder mice, thus no brain lesions were observed. On the other hand, in younger mice lesions were observed as the self-reactive cells attacked a similar position where the animal recovered from its infection.
During the observation of the infected areas of the brain cells, researchers found an accumulation of a certain type of immune cells called as brain resident memory T cells.
Professor Merkler explains, “Under normal circumstances, these cells are distributed throughout the brain, ready to protect it in case of a viral attack. But here, the cells accumulate in surplus at the exact spot of the infantile infection in the brain.”
The reason why brain lesions occurred in younger mice is that the brain resident memory T cells secrete a type of substance which gives the self-reactive cells access to the brain. Researchers confirmed the findings by blocking the receptor cells which were giving signals to the self-reactive cells. He says, “Indeed, the mice were then protected from developing brain lesions!”
Karin Steinbach adds, “We then looked to see if we could find a similar accumulation of brain-resident memory T cells that produce this molecule in people with multiple sclerosis, and indeed we did.”
After the analysis, researchers believe that the similar self-reactive T cells have access to the brain in humans too. This research provides a platform for future studies. Scientists hope that they will be able to reach the causes of multiple sclerosis soon.
Upon concluding the study, Karin Steinbach says, “We are continuing our research in this direction. We particularly want to understand why brain-resident memory T cells accumulate in these discrete spots in a child’s brain following infection but not in adulthood.”