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A specific immune response in pregnant mice leads to changes in the brain structure as well as the behavior of its offspring, just like humans with autism spectrum disorder (ASD), says a new study by University of Massachusetts researchers.

Moreover, the immune response reflects the occurrence of viral infections during human pregnancy. This supports earlier human studies showing links between maternal viral infections during pregnancy and the risk of autism in babies.

Due to a sudden shooting up in the interleukin-17a cytokine, stemming from a specific group of helper T cells (Th17), the inflammatory immune response in the mother led to the ASD symptoms in the offspring. It led to "repetitive behavior and abnormal communication" in the affected children. It was only when the action of Th17 cells was blocked that the normal structure and function was restored in the mice's brains.

"Blocking the function of Th17 cells and IL-17a in the maternal womb by using antibodies and other genetic techniques completely restored normal behavior and brain structure in the affected offspring," Jun Huh, co-author of the study, said in a press release.

"The study also showed that a therapeutic treatment with antibodies blocking IL-17a corrected certain behavioral abnormalities, suggesting Th17 cells, as well as the specific proteins they produce, may be a candidate therapeutic targets in efforts to prevent autism in the children of susceptible mothers," he added.

Whether these results can be replicated in human beings or not, and whether the Th17 cells undertake the same function in human mothers or not has to be determined by further research.

"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," said Dan Littman, another co-author of the study. He said that the results arrived at present are sourced only from viral infections and have no links with vaccinations at all.

The study will be published in the journal Science.