| First Author | Qin T | Year | 2025 |
| Journal | Neuron | Volume | 113 |
| Issue | 23 | Pages | 3983-4000.e7 |
| PubMed ID | 41027425 | Mgi Jnum | J:372915 |
| Mgi Id | MGI:8250705 | Doi | 10.1016/j.neuron.2025.09.001 |
| Citation | Qin T, et al. (2025) Treg-microglia partnership in the injured spinal cord preserves Treg cell function and regulates microglial cholesterol metabolism. Neuron |
| abstractText | The spatiotemporal dynamics and specific roles of regulatory T (Treg) cells in spinal cord injury (SCI) remain unclear. Using single-cell RNA sequencing, flow cytometry, and immunofluorescence, we found that thymus-derived Treg cells infiltrate the injured spinal cord via peripheral blood around 3 days post-SCI. Treg cell depletion worsened SCI and impaired long-term recovery. Transcriptomic profiling revealed strong anti-inflammatory functions of Treg cells and the potential to regulate cholesterol metabolism in neighboring microglia. Further single-cell RNA sequencing uncovered the clonality of SCI-associated Treg cells. Major histocompatibility complex class II (MHC II) expression on microglia, not macrophages, was crucial for sustaining Treg cell numbers and neuroprotective function, with myelin-phagocytosing microglia-activated Treg cells showing significant neuroprotective effects. Treg cells mitigated microglial inflammation via CTLA-4 and upregulated the ATP-binding cassette transporter G1 (Abcg1) receptor in microglia, helping to manage myelin load and reduce lipid droplet formation. Our findings offer mechanistic insights into SCI-associated Treg cells and lay the groundwork for future Treg-based therapies in SCI treatment. |
