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.
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.
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.