10.6084/m9.figshare.4970489.v1
Fagan K.
Fagan
K.
Crider A.
Crider
A.
Ahmed A.O.
Ahmed
A.O.
Pillai A.
Pillai
A.
Supplementary Material for: Complement C3 Expression Is Decreased in Autism Spectrum Disorder Subjects and Contributes to Behavioral Deficits in Rodents
Karger Publishers
2017
Complement system
Autism spectrum disorder
Immune system
Behavior
Rodents
2017-05-04 12:29:37
Journal contribution
https://karger.figshare.com/articles/journal_contribution/Supplementary_Material_for_Complement_C3_Expression_Is_Decreased_in_Autism_Spectrum_Disorder_Subjects_and_Contributes_to_Behavioral_Deficits_in_Rodents/4970489
<p>Autism spectrum disorder (ASD) is a neurodevelopmental disorder with
hallmark symptoms including social deficits, communication deficits and
repetitive behaviors. Accumulating evidence suggests a potential role of
the immune system in the pathophysiology of ASD. The complement system
represents one of the major effector mechanisms of the innate immune
system, and regulates inflammation, and orchestrates defense against
pathogens. However, the role of CNS complement system in ASD is not well
understood. In the present study, we found a significant increase in
C2, C5, and MASP1, but a decrease in C1q, C3, and C4 mRNA levels in the
middle frontal gyrus of ASD subjects compared to controls. Significant
decreases in the mRNA levels of 2 key proinflammatory cytokines, IL-17
and IL-23 were observed in ASD subjects. Our study further demonstrated a
strong association of complement genes with IL-17 and IL-23, suggesting
a possible role of the complement system in immune dysregulation in
ASD. We observed significant associations between complement components
and abnormality of development scores in subjects with ASD. In rodents,
C3 knockdown in the prefrontal cortex induced social interaction
deficits and repetitive behavior in mice. Together, these studies
suggest a potential role of C3 in the pathophysiology of ASD.</p>