Fig. 1

Neuroinflammatory response after ABI. Inflammation triggered by release of damage-associated molecular patterns (DAMPs) and reactive oxygen species (ROS) will cause activation of resident immune cells and release of proinflammatory citokines. Invasion of the CNS by circulating immune cells initially consists of innate immune cells, but is joined by adaptive leukocytes within days (primed T cells). While this response largely wanes, a proportion of patients display a persistent immune dysregulation, directly contributing to tissue damage. BBB blood brain barrier, DAMPS damaged associated molecular patterns, IL interleukin, iNOS inducible nitric oxide synthase, s100 calcium binding protein B (s100B); glial fibrillary acid protein (GFAP) neurofilament light (NFL); TGF transforming growth factor, TNF tumor necrosis factor. Figure created with BioRender.com