For Manuscript Submission, Check or Review Login please go to Submission Websites List.
For the academic login, please select your country in the dropdown list. You will be redirected to verify your credentials.
Maternal Immune Activation and Autism Spectrum Disorder: Interleukin-6 Signaling as a Key Mechanistic PathwayParker-Athill E.C.a–c · Tan J.a–c
aRashid Laboratory for Developmental Neurobiology, Silver Child Development Center, bDepartment of Psychiatry and Behavioral Medicine, cCollege of Medicine, University of South Florida, Tampa, Fla., USA Corresponding Author
Dr. Jun Tan
Department of Psychiatry, Silver Child Development Center
University of South Florida, 3515 E. Fletcher Ave.
Tampa, FL 33613 (USA)
Tel. +1 813 974 9326, Fax +1 813 974 3223, E-Mail firstname.lastname@example.org
An emerging area of research in autism spectrum disorder (ASD) is the role of prenatal exposure to inflammatory mediators during critical developmental periods. Epidemiological data has highlighted this relationship showing significant correlations between prenatal exposure to pathogens, including influenza, and the occurrence of ASD. Although there has not been a definitive molecular mechanism established, researchers have begun to investigate this relationship as animal models of maternal infection have support- ed epidemiological findings. Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals. These abnormalities have correlated with clinical findings of immune dysregulation, neurological and behavioral abnormalities in some autistic individuals. Additionally, researchers have observed genetic variations in these models in genes which regulate neurological and immunological development, similar to what is observed clinically in ASD. Altogether, the role of MIA and cytokine dysregulation, as a key mediator in the neuropathological, behavioral and possibly genetic irregularities observed clinically in autism are important factors that warrant further investigation.
© 2010 S. Karger AG, Basel