| Autor: |
Abou-El-Hassan, Hadi, Rezende, Rafael M., Izzy, Saef, Gabriely, Galina, Yahya, Taha, Tatematsu, Bruna K., Habashy, Karl J., Lopes, Juliana R., de Oliveira, Gislane L. V., Maghzi, Amir-Hadi, Yin, Zhuoran, Cox, Laura M., Krishnan, Rajesh, Butovsky, Oleg, Weiner, Howard L. |
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| Zdroj: |
Nature Communications; 7/18/2023, Vol. 14 Issue 1, p1-19, 19p |
| Abstrakt: |
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 (γδ) 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 γδ T cells affect the pathophysiology of TBI as early as one day and up to one year following injury in a mouse model. TCRδ−/− mice are characterized by reduced inflammation in acute TBI and improved neurocognitive functions in chronic TBI. We find that the Vγ1 and Vγ4 γδ T cell subsets play opposing roles in TBI. Vγ4 γδ T cells infiltrate the brain and secrete IFN-γ and IL-17 that activate microglia and induce neuroinflammation. Vγ1 γδ T cells, however, secrete TGF-β that maintains microglial homeostasis and dampens TBI upon infiltrating the brain. These findings provide new insights on the role of different γδ T cell subsets after brain injury and lay down the principles for the development of targeted γδ T-cell-based therapy for TBI. Traumatic brain injury is not only a neurological but also an immunological condition in which multiple innate and adaptive immune cell types play roles. Here authors show in a mouse model that the Vγ4 subtype of the unconventional gamma-delta T cells promote neuroinflammation, while the Vγ1 subtype ameliorates immunopathology. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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