Autism spectrum disorder, or ASD, is characterized by distinct abnormal behavioral changes, such as repetitiveness, communication difficulty, and lack of social skills. This disorder contains a broad spectrum of symptoms and behavioral difficulties which can vary greatly per individual (1). In recent years, autism has been linked to beginning as early as in the womb by initiating the mother’s immune system during pregnancy and/or producing antibodies that recognize fetal brain proteins as antigens and cause an immune response, leading to a loss of fetal brain proteins and inflammation (2).
The idea that the immune system can play a role in the development of autism within the womb began with observing hospitalized mothers. Data regarding pregnant mothers who were hospitalized due to a serious infection and the diagnosis of ASD in their offspring were analyzed to determine if correlation existed. The results show that viral infections of mothers in their first trimester and bacterial infections in the second trimester were associated with the development of ASD in their subsequent offspring (3). The results here support other experiments and is beneficial in that it uses human subjects that were exposed to disease by circumstance only, not purposely.
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Another study tested this idea by immune stimulation in pregnant rats. In a study performed in 2012, rat models that were in gestation were purposely infected to stimulate the immune system. The results show that the offspring displayed altered immune systems and function, with decreased levels of CD4+ TCR?+ Foxp3+ CD25+ T regulatory cells and heightened levels of IL-6 and IL-17 production by CD4+ T cells. These offspring also displayed similar behavioral symptoms to human ASD (4). At this point, the connection between the mother’s immune system and its ability to promote ASD in her offspring had been made, but the pathways of how it worked had yet to be discovered.
The presence of autoimmune diseases in the mother also can play a role in ASD development. Mothers who were diagnosed with at least one autoimmune disease, such as rheumatoid arthritis or type 1 diabetes, were more likely to have children diagnosed with ASD. This further links autism with the infection of a mother in gestation (5).
Mothers pass their own IgG isotype antibodies to their children within the womb, but they also can produce autism-associated maternal antibodies that specifically attack certain proteins within the brain of their unborn child. The presence of these antibodies has been linked to increased probability of the development of ASD in the child. One of the many studies that tested this pathway to why prenatal infection was correlated to ASD was focused on X. Women were tested for the presence of anti-fetal brain antibodies. Women who had immune systems that produced these antibodies also had decreased expression of the MET receptor tyrosine kinase led to behavioral changes in their offspring. This study also suggests that there is a predetermined genetic aspect to the production of self-reacting cytokines. A specific gene for MET receptor tyrosine kinase has been positively linked to the broken tolerance of the fetus, leading to the production of self-reacting antibodies. Decreased levels of regulatory cytokines, such as IL-10, also led to reduced MET expression, which could play a role in the development of ASD in the unborn child (6). This suggests that the development of ASD can begin as early as in the womb. Mothers could also be tested for the presence of these self-reacting antibodies and the presence of the gene that decreases expression of the MET receptor tyrosine kinase to determine the likelihood of producing a child with ASD.
When an immune response is initiated by a perceived antigen, an inflammatory state is produced in the affected area. Autism has been found to correlate with increased levels of inflammatory cytokines. In a study published in 2011, blood samples were drawn from three groups of children with an average age of 3.4 – children diagnosed with autism (ASD), children with early symptoms of ASD, and children with no onset of ASD as a control. The samples were tested by an ELISA assay to determine the quantitative presence of inflammatory cytokines. The results show that there is a distinct difference between the control group and the children diagnosed with ASD, with the majority of the children diagnosed with ASD having a significant increase in the levels of pro-inflammatory cytokines in serum. Post-mortem studies have also shown an increased level of inflammatory cytokines in the brain specifically, which could possibly be linked to the mother producing antibodies against the fetal brain during pregnancy (7).
In conclusion, many bounds have been made in the study of autism, how it is caused, and how it can be prevented. Definite links in the cause of autism has been made between the activation of a pregnant mother’s immune system during the early stages of pregnancy and the production of self-reacting antibodies against the fetal brain. Though there is a definite link between these pathways and the diagnosis of ASD in her subsequent offspring, there are broad arrays of causes to ASD, just as there is a broad array of symptoms within the spectrum of this disorder.
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