ALX, a TBK1 inhibitor, mitigated EAE development by inhibiting DC maturation and subsequent pathogenic Th1 and Th17 responses while increasing Treg responses through attenuating the TBK1/AKT and TBK1/IRF3 signaling.
Our data show that 1. autophagy defects can cause neuronal damage in EAE mice; and 2. curcumin may regulate the activation of autophagy in EAE mice by affecting the AKT/mTOR autophagy signalling pathway, further balancing central nervous system and peripheral autophagy.
The phosphoinositide-3-kinase (PI3K)-AKT kinase pathway modulates outcome during EAE, with direct actions of PI3K on adaptive immunity implicated in deleterious and effects on antigen presenting cells involved in beneficial responses during EAE.