The molecule that forms the basis for this study is a type of T helper cell called Th This warrior of the immune system produces a range of cytokines, one of which is interleukin 17a ILa. 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.
Th17, specifically, appears to be associated with multiple sclerosis , rheumatoid arthritis and psoriasis. And perhaps now, autism. To test the role of Th17 and ILa, 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. 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.
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 ILa and observed the effect on the offspring.
The team trialed two distinct methods of blocking the effects of ILa; one used anti-IL17a antibodies, and the other blocked the receptor responsible for the maturation of T cells and their consequent production of ILa.
Whichever method the team used to block ILa production, the resulting mice pups were now behaviorally normal. This is strong evidence that ILa plays an important role in these changes, but further work needs to be done to unpick the exact mechanisms behind the interaction. Littman says:. 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. Although there is variability in prevalence from community to community, the sites that report have been more or less consistent over time, so a review of the data trends for a specific site is enlightening, says Dr.
For example, at the ADDM community site in Utah, which covers Salt Lake City and surrounding counties, the prevalence of autism among 8-year-old Utah children has risen by nearly 30 percent in less than a decade.
University of Utah Health scientists attribute much of that rise to a heightened awareness of autism, better diagnostic tools to detect it, and improved access to medical care, according to a University of Utah Health press release. In several of the 11 communities the report described, including Utah, fewer Hispanic children were identified with autism than Black or white children.
This finding suggests that disparities in getting an ASD diagnosis due to ethnicity could be a problem, said Amanda Bakian, PhD , a coauthor of the study, an associate professor of psychiatry at the Huntsman Mental Health Institute at the University of Utah, and a principal investigator of the Utah ADDM study, in the release. Authors of the study also found that a higher percentage of Black children with autism were identified with intellectual disability compared with white or Hispanic children with autism.
If the prevalence of autism is truly increasing, increased awareness and referral for assessment and services can account for some of this, Klinepeter says. One possibility is that early exposure to a virus prods the body into mounting an immune response that somehow goes awry. In addition to producing antibodies against the virus, the body makes antibodies against itself, resulting in damage to tissues and organs. This "autoimmune" response is what happens in autoimmune diseases such as lupus, and some researchers think a similar response may account for the brain abnormalities found in people with autism.
In their study of 48 autistic children and 34 normal children and adults, the researchers measured levels of antibodies to two virusesmeasles virus and human herpesvirusin the subjects' blood.
These antibodies were chosen because they are often used in research on known autoimmune diseases, says Singh, the principal investigator of the project and an assistant research scientist in the College of Pharmacy. The researchers also measured levels of two brain autoantibodies antibodies to brain tissue. One, anti-MBP, is an antibody to myelin basic protein, a protein found in the protective sheaths around nerve fibers in the brain. The other, anti-NAFP, is an antibody to neuron-axon filament protein, a protein that makes up the nerve fibers themselves.
Virus antibody levels were essentially the same in autistic and non-autistic subjects, as the researchers expected. But the majority of autistic children who had virus antibodies also had brain autoantibodies. The higher the level of virus antibodies, the more likely an autistic child was to have brain autoantibodies. None of the non-autistic subjects had brain autoantibodies. The strongest link found in the autistic children was between measles virus antibodies and anti-MBP, suggesting that exposure to the measles virus may trigger an autoimmune response that interferes with the development of myelin, says Singh.
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