Akhirin Functions as an Innate Immune Barrier to Preserve Neurogenic Niche Homeostasis During Mouse Brain Development

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Authors: Mikiko Kudo, Tenta Ohkubo, T. Sugawara, Takashi Irie, Jun Hatakeyama, Shigehiko Tamura, Kenji Shimamura, Tomohiko Wakayama, Naoki Matsuo, Kinichi Nakashima, Takahiro Masuda, Kunimasa Ohta
Cited by: 2
References: 47

Abstract

Neurogenesis is tightly regulated by complex interactions among neural stem and progenitor cells (NSCs/NPCs), blood vessels, microglia, and extracellular matrix components within the neurogenic niche. In the embryonic brain, NSCs reside along the ventricular surface, where cerebrospinal fluid (CSF) directly regulates their proliferation. Here, we identify Akhirin (AKH) as a critical regulator that preserves the integrity of the NSC niche during mouse brain development. At embryonic day 14.5, AKH is secreted and enriched at the apical surface of choroid plexus epithelial cells and the ventricular lining. Loss of AKH leads to increases the inflammatory cytokine expression in the CSF and disrupts NSC niche homeostasis. Furthermore, AKH is cleaved upon inflammatory stimulation, and its LCCL domain directly binds bacteria, thereby preventing their spread. These findings reveal that AKH functions as a protective barrier molecule within the developing neurogenic niche, providing immune protection and preserving NSC niche homeostasis during periods when the innate immune defenses are still immature.

Fields of Study & Subjects

Neurogenesis and neuroplasticity mechanisms Neuroinflammation and Neurodegeneration Mechanisms Barrier Structure and Function Studies

Publication details

Journal / source
Cells
Publisher
MDPI AG
Volume
15
Issue
2
Pages
151–151
Publication date
14 January 2026
Language
EN