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Choroid Plexus Fibroblast-ILC2 Niche Promotes Adult Hippocampal Neurogenesis after Traumatic Brain Injury
Shiqi Gao1,2,3, Xiaoming Guo1,2,3, Sixuan Tian1,2,3
1Department of Neurosurgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Summary
Group 2 innate lymphoid cells (ILC2) accumulate in the choroid plexus after traumatic brain injury (TBI). ILC2 treatment improves TBI recovery by reducing inflammation and promoting neurogenesis.
Area of Science:
- Neuroimmunology
- Cellular Biology
- Trauma Research
Background:
- Immune signals from brain border tissues influence neural cells.
- Choroid plexus (ChP) structural changes and immune cell infiltration post-TBI are not well understood.
Purpose of the Study:
- Investigate ChP immune cell alterations after TBI.
- Determine the therapeutic potential of group 2 innate lymphoid cells (ILC2) in TBI recovery.
Main Methods:
- Single-cell RNA sequencing and histological analysis identified ILC2 accumulation in the ChP post-TBI.
- Intracerebroventricular adoptive transfer of ILC2 was used to assess its therapeutic effects.
- Single-nucleus RNA sequencing of the hippocampus analyzed ILC2-mediated neurogenesis.
Main Results:
- ILC2s were found to colonize the ChP and alleviate pathogenic immune infiltration during acute TBI.
- ILC2 treatment improved sensory-motor function and memory in chronic TBI.
- ILC2s, induced by IL33 from ChP fibroblasts, anchor via VCAM-1/Integrin α4β7.
- ILC2-derived AREG promoted hippocampal neurogenesis by interacting with EGFR.
Conclusions:
- Choroid plexus-resident ILC2s optimize the immune microenvironment post-TBI.
- ILC2s promote neurogenesis, offering a potential therapeutic strategy for TBI recovery.
