Discovery of Brain Immune Cells Involved in Autism Spectrum Disorder

Key Points

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with many unexplained mechanisms of onset. In recent years, the involvement of the brain and immune cells has been gaining attention.

Using an ASD model mouse, we discovered that γδ T cells, which produce IL-17A in the developing brain via CXCL16, accumulate and promote ASD-like social behavior abnormalities.

These findings offer a new perspective for understanding ASD not only from the nervous system but also from the interaction with the immune system, and are expected to lead to the development of new diagnostic and therapeutic methods targeting immune cells.

Abstract

Traditionally, Autism Spectrum Disorder (ASD) has been considered a neurodevelopmental disorder primarily caused by abnormalities in neurons and neural circuits. In recent years, however, the possibility that changes in the immune system, such as infections and inflammation during pregnancy, may affect brain development and behavior has been drawing attention. However, it has not been fully understood how immune cells act on the brain and contribute to abnormalities in social behavior in genetically based ASD.

A research group has now elucidated a new mechanism in model mice that replicate chromosomal abnormalities associated with ASD, where specific immune cells accumulate in the developing brain and promote abnormalities in social behavior.

The research group, including Associate Professor Minako Ito and graduate student Natsumi Takayama (at the time) from the Kyushu University Medical Institute of Bioregulation, Professor Toru Takumi from Kobe University, Professor Manabu Makinodan from Kumamoto University, Professor Kazuhiko Yamamuro from Nara Medical University, and Professor Akira Makino from Hamamatsu University School of Medicine, analyzed the brains of ASD model mice during development and discovered that a larger number of γδ T cells than usual accumulate in the brain. Furthermore, they revealed that CXCL16, produced by microglia (immune cells in the brain), attracts γδ T cells to the brain. The γδ T cells that accumulated in the brain produced IL-17A, a substance involved in inflammation. Additionally, suppressing the activity of γδ T cells and IL-17A with antibodies improved the abnormalities in social behavior observed in the ASD model mice.

This discovery provides a new perspective for understanding ASD not as a disorder solely of neurons, but from the interaction between the brain and immune cells. It is expected to be useful in the future for the development of new diagnostic and therapeutic methods for ASD targeting brain immune cells and IL-17A signaling.

This research was published in the American scientific journal "Science Immunology" on June 19, 2026 (US Eastern Time).

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Published Paper

Journal: Science Immunology Paper Title: CXCL16-mediated recruitment of γδ T cells to the brain reduces sociability in mice Authors: Natsumi Takayama, Koyomi Shiraishi, Ako Matsui, Shinya Hatano,

Kazuhiko Yamamuro, Kenta Nitahara, Akira Makino, Tatsuya Yokota, Nesta Amagiri,

Mahiro Watanabe, Ayame Nagafuchi, Mio Kawazoe, Minami Serino, Yoshihiro Harada, Tomoaki Takao, Kakeru Takenobu, Yasunobu Yoshikai, Kazufumi Kunimura,

Manabu Makinodan, Toru Takumi, Minako Ito DOI: 10.1126/sciimmunol.adz8466

Contact Information

<Regarding Research>

Kazuhiko Yamamuro

Director and Professor, Health Care Center and Department of Psychiatry, Nara Medical University

TEL: 0744-22-3051 FAX: 0744-29-8811

E-mail: muro@naramed-u.ac.jp *Please replace ""AT"" with @.

Minako Ito

Associate Professor, Medical Institute of Bioregulation, Kyushu University

TEL: 092-642-6965 FAX: 092-642-6965

Mail: ito.minako.719@m.kyushu-u.ac.jp *Please replace ""AT"" with @.

<Regarding Media>

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