Although several observations from earlier had suggested a connection between the immune system and the nervous function – due to the discovery that psychological stress lowers the healing rate of wounds – it was not until the 70s that the connection became more significant. During that decade, the American psychologist, Robert Ader, founded the field of ‘psychoneurobiology’ as he showed that immune response could be conditioned in rats. Since conditioning is learning, it involves increased brain centres, and therefore there had to be a connection between the immune system and the brain. It is, among other things, also what is seen with the placebo effect – patients on certain drugs or methods with no medically proven effect, but where the patients felt better afterwards. In 2009, Adler showed that the placebo effect had significant importance for the treatment of psoriasis.
A study from 2016 by Jonathan Kipnis – Ph.D., chairman of UVA Institute of Neuroscience – revealed additional connections between the brain and the immune system. He discovered connections between the vessels in the membranes of the brain (layers of tissue that cover the central nervous system) and the lymphatic system (a transportation system for the cells of the immune system). This discovery contradicted the general understanding of the brain being ‘immune privileged’ – it could tolerate pathogens without forming an anti-inflammatory immune response – and that it lacked direct communication between the two systems. Kipnis’ latest endeavour even more clearly illustrates a brain-immune-interaction. His research team found that an immune molecule (interferon-gamma) could be of major significance in social behaviour.
Usually, Interferon-gamma is released in response to a pathogenic attack, regardless of it being a virus, bacteria or parasite. However, a number of animals, herein zebrafish, flies, rats and mice have also shown to activate Interferon-gamma, when they become social. In the new study from Kipnis, researchers blocked Interferon-gamma to understand its effect on the brain of mice. This blockage was conducted using genetic modification, and this caused hyperactivity in the brain of the mice. They became significantly less social, and as soon as the molecule was introduced, the brain’s activity returned to normal, and the mice became social again. These discoveries suggest that the immune system plays a larger role in the social behaviour. Anthony J. Filiano – co-author of this study – adds an important remark. He points out that being social is very important for an organism to survive. It is important to seek food, sexual reproduction, assembling and hunting. Therefore, he assumes that organisms are more inclined to spread disease when being social. This means that you need to socialise, but that your risk of spreading pathogens increases as a result.
The idea is that Interferon-gamma in evolution has been used as a more effective way of seeking out social behaviour, while also strengthening an anti-pathogenic response. According to the scientists, it is possible that a disturbed immune system could be involved in the social problems associated with neurological and psychiatric disorders. This research is the first step within a field that seems to have plenty of new discoveries.
The consequences of autism and other conditions can be immense, but this is still too early to tell. Given the fact that both neuroscience and immunology are extremely complicated fields of study, it will take a long time to explore these and thus fully understand their interaction with each other. There is no single molecule responsible for a condition with a social dysfunction, but the discovery of the immune system – thus also the bacteria – having a certain influence on social interaction, opens completely new and exciting ways of innovative actions.
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