New research published in Science demonstrates a connection between a mother’s immune response to a viral threat and autism-like traits in the offspring of mice.

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New research investigating the root of autism implicates T helper cells.

Despite first being described in 1943, autistic spectrum disorders remain a mysterious affliction.

Autism affects an estimated 1 in 68 American children, but the exact mechanisms at fault are still very much up for debate.

One avenue of research has shown links between viral infections in the mother during pregnancy and an increased risk of autism in the child.

A new study, taking a fresh look at the immune response, has identified a subsection of immune cells that appear to cause certain behaviors linked to autism.

Dr. Dan Littman and his team of researchers from NYU Langone Medical Center, Massachusetts Institute of Technology, University of Massachusetts Medical School and the University of Colorado focused their sights on a specific immune response that deals with viral invaders.

Dr. Littman says:

To our knowledge, this is the first study to identify a specific population of immune cells that may have a direct role in causing behaviors linked to autism.”

He also preempts discourse on the potential confusion between his work and the effects of vaccines on autism. He makes it clear that his work looking at the impacts of viruses has “nothing whatsoever to do with vaccines.”

The molecule that forms the basis for this study is a type of T helper cell called Th17. This warrior of the immune system produces a range of cytokines, one of which is interleukin 17a (IL-17a).

T helper cells are major players in the immune orchestra; they release cytokines that amplify the immune response when necessary and help suppress or regulate it to prevent overactivity. In moments of error, they also contribute to autoimmune diseases, where the body’s defenses turn inward.

Th17, specifically, appears to be associated with multiple sclerosis, rheumatoid arthritis and psoriasis. And perhaps now, autism.

To test the role of Th17 and IL-17a, the team triggered their production by mimicking a viral invasion in pregnant mice.

They then monitored the mouse babies and assessed whether they showed behavioral abnormalities. Ultimately, they found that the resultant offspring showed distinct autism-like traits.

The researchers noted that the Th17 babies could not tell the difference between other mouse pups and a toy mouse, spending equal time with both. “Normal” mouse pups preferentially spend time with real mice, rather than toys.

Th17 offspring had measurably different vocalizations when crying to their mothers, and, when marbles were left in their cages, the Th17 pups buried them one after the other in an orderly, compulsive fashion.

On dissection, the team found that the IL-17a had impacted the development of the mouse pups’ brains. Certain sections of the cortex, responsible for making sense of sights and sounds, were chaotically ordered. These types of cortical disorganization have previously been found in other autism models.

For the next phase of experimentation, the team once again stimulated the pregnant mice to generate the anti-virus response, but this time, they blocked the action of IL-17a and observed the effect on the offspring.

The team trialed two distinct methods of blocking the effects of IL-17a; one used anti-IL17a antibodies, and the other blocked the receptor responsible for the maturation of T cells and their consequent production of IL-17a.

Whichever method the team used to block IL-17a production, the resulting mice pups were now behaviorally normal.

This is strong evidence that IL-17a plays an important role in these changes, but further work needs to be done to unpick the exact mechanisms behind the interaction. Dr. Littman says:

What is needed next is a study of viral infection during pregnancy that follows thousands of women, tracking instances of viral infection or flare-ups in autoimmune conditions and the diagnosis of autism spectrum disorder in children over several years.

Only such a study could determine if there is increased incidence of autism in the children of mothers who reported an inflammatory event in a given part of gestation.”

Although Dr. Littman and colleagues have patented their methods of blocking IL-17a’s actions, it will be years before they can be converted into a usable human treatment to prevent autism. Also, because of the wide array of autistic types, it may well be that the immune response is only a part of the entire picture.

The study certainly yields fascinating results; the scientific community waits with baited breath for the next round of investigations. Medical News Today recently covered research investigating certain genetic mutations that might cause autism.