Background and Purpose:
Traumatic brain injury (TBI) remains a major public health concern
worldwide with unmet effective treatment. Stimulator of Interferon Genes
(STING) protein and its downstream type-I Interferon (IFN) signaling are
now appreciated to be involved in TBI pathogenesis. Compelling evidence
have shown that STING and type-I IFNs are key in mediating detrimental
neuroinflammatory response after TBI, exacerbating outcome. Therefore,
pharmacological inhibition of STING presents a viable therapeutic
opportunity in combating the detrimental neuroinflammatory response
after TBI.