| First Author | Somebang K | Year | 2021 |
| Journal | Cell Rep | Volume | 36 |
| Issue | 12 | Pages | 109727 |
| PubMed ID | 34551293 | Mgi Jnum | J:334262 |
| Mgi Id | MGI:6876889 | Doi | 10.1016/j.celrep.2021.109727 |
| Citation | Somebang K, et al. (2021) CCR2 deficiency alters activation of microglia subsets in traumatic brain injury. Cell Rep 36(12):109727 |
| abstractText | In traumatic brain injury (TBI), a diversity of brain resident and peripherally derived myeloid cells have the potential to worsen damage and/or to assist in healing. We define the heterogeneity of microglia and macrophage phenotypes during TBI in wild-type (WT) mice and Ccr2(-/-) mice, which lack macrophage influx following TBI and are resistant to brain damage. We use unbiased single-cell RNA sequencing methods to uncover 25 microglia, monocyte/macrophage, and dendritic cell subsets in acute TBI and normal brains. We find alterations in transcriptional profiles of microglia subsets in Ccr2(-/-) TBI mice compared to WT TBI mice indicating that infiltrating monocytes/macrophages influence microglia activation to promote a type I IFN response. Preclinical pharmacological blockade of hCCR2 after injury reduces expression of IFN-responsive gene, Irf7, and improves outcomes. These data extend our understanding of myeloid cell diversity and crosstalk in brain trauma and identify therapeutic targets in myeloid subsets. |
