〇 Autism spectrum disorder (ASD) is a neurodevelopmental condition with many aspects of its pathogenesis still unclear. Recently, interactions between the brain and immune cells have attracted increasing attention. 〇 Using a mouse model of ASD, researchers discovered that γδT cells producing IL-17A accumulate in the developing brain via CXCL16 signaling, promoting ASD-like social behavioral abnormalities. 〇 This finding provides a novel perspective on understanding ASD not only from a neurological standpoint but also through interactions between the nervous and immune systems, offering potential for developing new diagnostic and therapeutic approaches targeting immune cells. (Overview) Traditionally, autism spectrum disorder (ASD) has been considered primarily a neurodevelopmental disorder caused by abnormalities in neurons and neural circuits. In recent years, however, changes in the immune system—such as maternal infection or inflammation during pregnancy—have been recognized as potentially affecting brain development and behavior. Nevertheless, how immune cells influence brain function and contribute to social behavioral abnormalities in genetically based ASD has remained poorly understood. In this study, a research group revealed a novel mechanism in a mouse model of ASD that recapitulates chromosomal abnormalities associated with human ASD: specific immune cells accumulate in the brain during development and promote abnormal social behaviors. The research team, led by Associate Professor Minako Ito of the Research Institute for Microbial Diseases at Osaka University, graduate student Natsumi Takayama (at the time), Professor Toru Takumi of Kobe University, Professor Manabu Makinodan of Kumamoto University, Professor Kazuhiko Yamamuro of Nara Medical University, and Professor Akira Makino of Hamamatsu University School of Medicine, analyzed the brains of ASD model mice during development and discovered an increased presence of γδT cells compared to normal mice.