Research carried out by the biopharmaceutical company Immune Response Corporation suggests that FOXP3, a specific genetic marker on T-cells, is significantly reduced in patients with multiple sclerosis compared to healthy controls.
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Clinical research conducted by the company in association with Oregon Health & Science University (OHSU) indicates that FOXP3, known to be involved in maintaining immune tolerance and regulation of autoimmune diseases, is depleted in patients with multiple sclerosis (MS).
There findings are significant because deficiency of FOXP3 in MS patients is said to be linked to deficient numbers of regulatory T-cells. Immune Response believes that induction of these – cells is important to the mechanism of action for NeuroVax, the company’s peptide immune-based therapy.
Autoimmune diseases such as MS may result from the failure of tolerance mechanisms to prevent expansion of pathogenic T-cells. This research establishes that MS patients have abnormalities in FOXP3 message and protein expression levels in peripheral T-cells.
This observation is the first to link a defect in functional peripheral immunoregulation to an established genetic marker, FOXP3. Diminished FOXP3 levels indicate impaired immunoregulation by Treg cells that may contribute to MS.
It is hoped that further research may facilitate the development of novel therapeutic approaches to treating MS.