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Poster - VDR Nuclear Receptor competence is the key to recovery from chronic inflammatory and autoimmune disease

Type: Abstract presentation
Presented by: Trevor Marshall, PhD
Conference: Days of Molecular Medicine 2006
Location: Karolinska Institute
Date: 2006
Additional content: PDF of Poster

Abstract

The VDR Nuclear Receptor is at the heart of the human innate immunity, responsible for TLR2, TLR4, CAMP TACO and IL2 expression [1]. During Th1 immune challenge, the VDR is activated by the endogenous secosteroid 1,25 dihydroxyvitamin D. We have previously described how intra-phagocytic bacterial pathogens are responsible for much chronic inflammatory disease [2,3], and our phase 2 study results have confirmed this pathogenesis. In order to induce recovery from chronic inflammatory disease, it is necessary to restore VDR function by removing all exogenous sources of the secosteroid we call ‘Vitamin-D,’ and dampen down over-exuberant VDR activity, for example with the ARBA drug which is an angiotensin receptor blocker. One of the ARBs is olmesartan (Benicar). Not all ARBs activate the Vitamin D Receptor. Olmesartan[1]. This enables the immune system to recognize the pathogens.

RESULTS: To date we have demonstrated recovery from Hashimoto’s Thyroiditis, Rheumatoid Arthritis, Sarcoidosis, and an assortment of chronic inflammatory diagnoses. This breakthrough is the result of a collaboration between molecular scientists and a disparate group of innovative physicians, facilitated by the Internet. However, the widespread application of this pathogenic understanding will require meticulous translation of the molecular science into conventional clinical precepts.

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