NF-kappaB plays a central role in triggering relapse in multiple sclerosis
The reason for relapse in multiple sclerosis is unknown.
The researchers identified 43 genes that were differently expressed during acute relapse vs. complete remission. After analyzing these differences they conclude that NF-kB plays a central role in triggering relapse.
This is consistent with the theory that a pro-inflammatory state (common to most individuals in the Western world) leads to chronic over activation of NF-kB. In combination with genetic vulnerability, autoimmune disease can manifest.
By restoring the proper balance between inflammation inhibitors and inflammation promoters, this pro-inflammatory state might be relieved. NF-kB might then no longer be chronically over-activated, which might lessen the chance of relapse in multiple sclerosis.
Molecular network analysis of T-cell transcriptome suggests aberrant regulation of gene expression by NF-kappaB as a biomarker for relapse of multiple sclerosis.
Summary of the abstract
The reason for acute relapse in multiple sclerosis is unknown.
The aim of this study was to identify the specific genes in T lymphocytes that might be responsible for causing relapse.
A set of 43 differentially expressed genes was identified – genes that varied between acute relapse and complete remission. Analysis then showed the most significant relationship with NF-kB in T cells during relapse of multiple sclerosis.
These results suggest that NF-kB plays a central role in triggering the events leading to relapse.