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Published on: March 25, 2016
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IL-6 Inhibition Partially Ameliorates Maternal Immune Activation-Induced Autism-Like Behavioral Abnormalities in
Xiaoyun Zhang1, Weili Luo2, Kaiyue He3
1Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan 528400, China.
Current Issues in Molecular Biology
|October 28, 2025
Summary
Prenatal immune activation linked to autism spectrum disorder (ASD) may cause anxiety. Targeting interleukin-6 (IL-6) partially improved social behaviors and reduced anxiety in a mouse model, but did not fully reverse core ASD traits.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Prenatal maternal immune activation (MIA) is linked to autism spectrum disorder (ASD) pathogenesis.
- Interleukin-6 (IL-6) is a key inflammatory mediator implicated in MIA's effects.
- Toxoplasma gondii soluble tachyzoite antigen (STAg) is used to induce MIA in experimental models.
Purpose of the Study:
- To investigate the therapeutic potential of IL-6 inhibition in an MIA mouse model.
- To assess the impact of IL-6 blockade on anxiety-like and ASD-like behaviors in adult offspring.
Main Methods:
- Induced MIA in mice using STAg.
- Administered IL-6-neutralizing antibody (MP5-20F3) or isotype control to adult MIA offspring.
- Conducted behavioral assessments including open field, elevated plus maze, reciprocal social interaction, and three-chamber tests.
Main Results:
- STAg-induced MIA offspring exhibited heightened anxiety-like behaviors, which were largely reversed by IL-6 inhibition.
- Diminished sociability in STAg offspring was partially restored by IL-6 inhibition.
- Core ASD-like features, including social preference deficits and repetitive behaviors, were resistant to IL-6 inhibition.
Conclusions:
- Systemic IL-6 inhibition partially ameliorates anxiety-like and social interaction deficits in an MIA mouse model.
- IL-6 plays a significant role in specific behavioral abnormalities associated with MIA.
- Targeting IL-6 may address a subset of ASD-related symptoms, but comprehensive strategies are necessary for broader efficacy.
