The Janus face of NK cells in neurodevelopment.

This research review looks at how immune system cells called NK cells might contribute to autism development. When mothers experience infections or inflammation during pregnancy, it may activate these immune cells in ways that affect brain development in their babies. The researchers suggest that NK cells work with brain immune cells to potentially increase autism risk, though exactly how this happens isn't fully understood yet.

This review examines the role of natural killer (NK) cells in neurodevelopmental disorders, particularly autism spectrum disorder. The authors explore how maternal immune activation during pregnancy may contribute to autism risk through NK cell dysfunction. The review synthesizes evidence from clinical studies and animal models, highlighting microglia as a central component in immune-mediated neurodevelopmental changes. The authors propose that aberrant NK cell activation may contribute to autism pathogenesis through interactions with brain immune cells, though the specific mechanisms remain unclear.

The review calls for further research to understand NK cell-microglia interactions to inform future preventive and therapeutic approaches.

Understanding NK cell involvement in autism may lead to new prevention strategies during pregnancy and novel therapeutic targets. However, translation to clinical practice requires further mechanistic research and validation in human studies.

This is a review paper that synthesizes existing research rather than presenting new data. The underlying mechanisms linking NK cells to autism remain poorly defined. The clinical evidence appears limited to observational studies and animal models.

Maternal immune activation (MIA), triggered by infection or inflammation during pregnancy, is a well-recognized risk factor for neurodevelopmental disorders (NDDs) such as autism spectrum disorder (ASD). Clinical cohort studies and rodent models suggest that natural killer (NK) cells play a significant role in NDD pathogenesis, but the underlying mechanisms remain poorly defined. Here, we summarize the key immune mediators involved in MIA-induced NDDs, emphasizing microglia as a central hub. We then examine emerging evidence implicating aberrant NK cell activation in ASD, underscoring their overlooked contribution to impaired neurodevelopment.

Finally, we discuss potential mechanisms of NK cell-microglia crosstalk in NDDs. Elucidating these interactions in the context of MIA will be crucial for developing preventive and therapeutic strategies against inflammation-driven NDDs.