Experimental autoimmune encephalomyelitis: Association with mutual regulation of RelA (p65)/NF-κB and phospho-IκB in the CNS

► The phosphorylation of RelA's inhibitory factor IκB and subsequent RelA activation are important to the disease process of EAE. ► The expression of RelA and phospho-IκB was markedly increased in the initiation and during the progression of EAE. ► TPCK-treated EAE mice showed lower incidence of EAE with less severe symptoms and quicker recovery than vehicle-treated EAE mice. ► TPCK significantly suppressed the MOG35-55-specific T cell proliferation by reducing the production of IFN-γ and IL-17 cytokines in EAE. ► The NF-κB cascade's activity increased gradually with the development of symptoms and brain pathology of EAE.