Fig. 3

Bile pigments and encephalomyelitis. In encephalomyelitis, BR acts an important immunomodulator through multiple mechanisms, especially in T cell reactivity. BR inhibits STAT-1 and IκB phosphorylation, which are essential for CIITA and NF-κB activation in T cell activation. BR also achieves this via suppressing the upregulation of CD28, B7-1, and B7-2, and scavenging of ROS. Furthermore, BR treatment notably decreases the production of Th-1, Th-2, and Th-17 cytokines. Through these mechanisms, BR is thought to suppress T cell reactivity and act as a therapeutic agent in encephalomyelitis. (BR: bilirubin, NF-κB: nuclear factor kappa B, ROS: reactive oxygen species, Th: T helper cell)