Scientists hail “profound” discovery: Findings support theories pointing to immune response as factor in Autism and other complex conditions.
A new study, published in the journal Nature (Filiano A J et al**) reports the discovery of indicators suggesting that the immune system can affect, and may even control, our social behaviour.
The research, conducted at the University of Virginia School of Medicine, revealed that the blocking of a single immune molecule rendered mouse brains hyperactive, and led to a reduction in social behaviour. These effects were reversed when blocking of the molecule was lifted.
The new discovery, hailed by scientists as being of “profound” importance to social functioning research, is set to trigger new discoveries on a range of neurological conditions. Amongst conditions set to benefit most are autism, schizophrenia and depression, for which inflammatory or auto-immune factors have been posited as possible contributory factors.
Speaking to science media, Dr John Kipnis, chairman of the University’s Department under whose aegis Filiano et al conducted their research, explained the significance of the finding:
“…some of our behaviour traits might have evolved because of our immune response to pathogens,” added that, “…maybe we are just multicellular battlefields for two ancient forces: pathogens and the immune system. Part of our personality may actually be dictated by the immune system.”
Filiano and colleagues’ findings follow hot on the heels of an earlier, paradigm-busting discovery, that came out of the same Virginian research centre just last year. In that pioneering study, the investigators found a direct link between the brain and the lymphatic system.
This completely up-ended decades of clinical orthodoxy, which held that no such link exists, and helped lay the groundwork for Filiano et al’s discovery of a link between the immune system and social behaviour.
More specifically, what Filiano’s team reported is that the immune factor, interferon-gamma (a cytokine secreted by T lymphocytes) is activated in mice when they engage in social behaviour. Until this discovery, it had been believed that production of interferon-gamma was normally only triggered by an assault on the immune system by pathogens.
Further, Filiano’s team also reported that blocking interferon-gamma led to hyperactivity and an accompanying reduction in social behaviour in their mice subjects; whilst lifting the block served to restore the mice’s sociability.
Quoted by online media, Dr Anthony Filiano, observed that social behaviour is key to a species survival, not only in the search for food and drink but also to successful sexual reproduction and, he continued: “…the hypothesis is that when organisms come together, you have a higher propensity to spread infection. So you need to be social, but you [also] have a higher chance of spreading pathogens. The idea is that interferon gamma, in evolution, has been used as a more efficient way to both boost social behaviour while [also] boosting an anti-pathogen response.”
Implications for Autism and other neurological conditions
These findings raise the possibility that dysfunctions in the immune system may account for the social deficits which are present in a range of neurological and psychiatric disorders.
To be clear, there is no suggestion that a particular immune molecule may be responsible for complex presentations like autism, schizophrenia or depression.
However, it does seem entirely reasonable to postulate a role for the immune system and, in turn, perhaps even particular pathogens – as possibly significant factors in the genesis of a range of complex disorders that have a significant social component in their presentation.
**Filiano A. J. et al. Unexpected role of interferon-gamma in regulating neuronal connectivity and social behaviour. Nature: 535, 425–429 (Published online 13 July 2016).
This post also includes quotes from study contributors, as carried by the University of Virginia online news portal, UVA Today, and by online science news outlets Neuroscience News and Science Daily.