| First Author | Abou-El-Hassan H | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 4286 |
| PubMed ID | 37463881 | Mgi Jnum | J:338322 |
| Mgi Id | MGI:7510622 | Doi | 10.1038/s41467-023-39857-9 |
| Citation | Abou-El-Hassan H, et al. (2023) Vgamma1 and Vgamma4 gamma-delta T cells play opposing roles in the immunopathology of traumatic brain injury in males. Nat Commun 14(1):4286 |
| abstractText | Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. The innate and adaptive immune responses play an important role in the pathogenesis of TBI. Gamma-delta (gammadelta) T cells have been shown to affect brain immunopathology in multiple different conditions, however, their role in acute and chronic TBI is largely unknown. Here, we show that gammadelta T cells affect the pathophysiology of TBI as early as one day and up to one year following injury in a mouse model. TCRdelta(-/-) mice are characterized by reduced inflammation in acute TBI and improved neurocognitive functions in chronic TBI. We find that the Vgamma1 and Vgamma4 gammadelta T cell subsets play opposing roles in TBI. Vgamma4 gammadelta T cells infiltrate the brain and secrete IFN-gamma and IL-17 that activate microglia and induce neuroinflammation. Vgamma1 gammadelta T cells, however, secrete TGF-beta that maintains microglial homeostasis and dampens TBI upon infiltrating the brain. These findings provide new insights on the role of different gammadelta T cell subsets after brain injury and lay down the principles for the development of targeted gammadelta T-cell-based therapy for TBI. |
