Inhibition of NF-kB was found to be effective in preventing relapse in a mouse model of multiple sclerosis.

The publication:

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J Autoimmun. 2000 May;14(3):205-11.

Treatment of established relapsing experimental autoimmune encephalomyelitis with the proteasome inhibitor PS-519.

Vanderlugt CL, Rahbe SM, Elliott PJ, Dal Canto MC, Miller SD.

Departments of Microbiology-Immunology, 38 Sidney Street, Cambridge, MA 02139, USA.

Summary of the abstract

PLP139-151-induced relapsing experimental autoimmune encephalomyelitis (R-EAE) in SJL mice is a Th1-mediated autoimmune demyelinating disease model for multiple sclerosis (MS) in which the primary disease relapse is mediated by T cells specific for the endogenous PLP178-191 epitope.

This complex inflammatory process requires the co-ordinated expression of a wide variety of immune-related genes active at a variety of stages of the autoimmune process which are regulated, in part, by the transcription factor nuclear factor (NF)-kappaB (NF-kB).

The purpose of this study was to determine the effect of NF-kB inhibition in the mouse model.

NF-kB inhibition during the remission phase, following acute clinical disease was effective in significantly reducing the incidence of clinical relapses and CNS changes.

The inhibition of clinical disease was dependent upon continuous NF-kB inhibition.

The data suggest that NF-kB inhibition may offer a novel and efficacious approach for the treatment of progressive autoimmune diseases, including MS.

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