Figure 2.

T cell–NVU interactions in ICH. Experimental studies show that infiltrating CD4+ T lymphocytes are rapidly activated and recruited to the hemorrhagic brain accumulating in the peri-hematomal regions. (a). Infiltrated T cells contribute to the inflammatory environment of the injured brain by releasing a battery of cytokines and are a factor in the recruitment of other peripheral leukocytes via chemokine release and endothelial interactions. (b). T cells interact with many NVU component cells; astrocytes, pericytes, and microglia can be activated and polarized towards a pro-inflammatory state. T cells can activate endothelial cells, cause their dysregulation, and directly cause endothelial apoptosis. (c). T cells damage the BBB by amplifying inflammation and reducing the expression of major tight junction proteins. The sum of these actions increases PHE and harmful inflammation to contribute to the progression of secondary ICH injury, which worsens outcomes.