Findings Show Aberrant Innate Cellular Function, Neuroinflammation, and Microglia Activation Could Lead to Irregular Neurodevelopment
Researchers from the MIND Institute at UC Davis recently published a comprehensive review presenting current findings of innate immune dysfunction found in autism spectrum disorder (ASD). The authors found growing evidence that innate immune dysfunction plays a role in the etiology of ASD and found issues surrounding innate cellular function, neuroinflammation and microglia activation. Specifically, the team discovered that innate immune activation is evident in the periphery of those with ASD. This activation is linked to increased behavioral impairment. The authors also found that activation of microglia and increased innate immune cytokines have a basis in neuroinflammation discovered in autism brain specimens. However, the team reported that the underlying cause(s) of abnormal neurodevelopment and immune dysfunction observed in ASD remains unknown. But they indicate that the chronic immune dysregulation identified in the disorder is likely influenced by mechanisms that govern long-term cellular phenotype and behavior. For example, the authors point to epigenetic modifications involved in trained immunity that could be skewing myeloid cells toward an activated state, or alterations in the development of hematopoietic stem cells into myeloid cells that could be skewed. They suggest that future studies must consider the heterogeneity of ASD when looking into the etiology and integrate the immune system’s role in that search. The authors demonstrated optimism about studies that successfully identified subgroups of ASD children based on particular innate immune signatures. Ultimately, the team believes that further research and the use of unbiased technological approaches will aid in the understanding of how the innate immune system can be used to characterize ASD heterogeneity, which some day may improve potential personalized therapeutic strategies and the quality of life for autistic people and their families.
