Multiple sclerosis due to childhood viral diseases

Researchers at the Université de Genève have gained new insights into multiple sclerosis. In one study, they identified a potential link between viral infections in childhood and an increased risk of autoimmune diseases in adulthood.

Early childhood infections can lead to autoimmune diseases

Researchers at the Université de Genève have gained new insights into multiple sclerosis. In one study, they identified a potential link between viral infections in childhood and an increased risk of autoimmune diseases in adulthood.

In a mouse study conducted by the University of Geneva (in French: Université de Genève or UNIGE) and the Geneva University Hospital (in French: Hôpitaux Universitaires de Genève or HUG), researchers investigated the relationship between cerebral viral infections in childhood and the occurrence of multiple sclerosis in adulthood. The scientists found changes in the brain caused by the infection, which occur many years later in precisely the infected areas and cause damage to the autoimmune system.

According to current results, 2,221,188 people worldwide were affected by multiple sclerosis in 2016. Professor Doron Merkler explains the background of the new study: "We have asked ourselves whether viral brain diseases in early childhood could be one of the causes of the disease if it is the case that multiple sclerosis occurs at the age of about 30 years. He adds: "Under certain circumstances, transient infections can leave their inflammatory footprint in the brain."

Childhood as a decisive phase in the risk of disease

To test their hypothesis, the researchers injected transient virus infections into a group of adult mice and a group of young mice. Karin Steinbach explains: "In both cases, the mice showed no symptoms and both groups recovered within one week by means of comparable immune reactions".

When the mice were older, self-reactive cells were administered to both groups. Steinbach explains this process: "Most of us have self-reactive cells. But since they are controlled by regulatory mechanisms and do not normally have access to the brain, they do not always have to be associated with diseases."

In the mice injected with the virus in adulthood, the self-reactive cells could not access the brain and no brain damage could be detected. However, in mice infected at a young age, the reactive cells migrated to the brain. They occurred in exactly the same places where the infections had occurred before. Therefore, the reactive cells in the young mice attacked the affected brain structure and caused brain lesions.

Accumulated T cells as a signal

While examining the brains, the researchers identified the accumulations of T-memory cells in the young mice group. "Normally, these cells are distributed throughout the brain to protect it from viral attacks. But here they occur in abundance at the sites where the childhood infection took place," notes Professor Merkler.

The T-memory cells produce a molecule that attracts the self-reactive cells, and in particular, allows them to enter the brain and thus causes brain lesions. Merkler explains: "In order to confirm these observations, we blocked the receptor that transmits the signal to the self-reactive cells. In this case, the mice were protected from the development of brain lesions!"

Similar observations in humans

"When we examined people with multiple sclerosis, we found that there was a very similar accumulation of T memory cells that produced this molecule," notes Karin Steinbach. The researchers, therefore, believe that self-reactive T cells can enter the brain in humans through mechanisms similar to those in mice.

Steinbach concludes: "We are currently continuing our research in this direction. We want to understand why T-memory cells accumulate in children's brains after infections, but not in adults". In the future, the knowledge gained from the study could lead to a better understanding of the basics of multiple sclerosis.

Source:
Brain-resident memory T cells generated early in life predispose to autoimmune disease in mice. Karin Steinbach, Ilena Vincenti, Kristof Egervari, Mario Kreutzfeldt, Franziska van der Meer, Nicolas Page, Bogna Klimek, Irène Rossitto-Borlat, Giovanni Di Liberto, Andreas Muschaweckh, Ingrid Wagner, Karim Hammad, Christine Stadelmann, Thomas Korn, Oliver Hartley, Daniel D. Pinschewer and Doron Merkler. Science Translational Medicine 26 Jun 2019: Vol. 11, Issue 498, eaav5519. DOI: 10.1126/scitranslmed.aav5519

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