Aryl Hydrocarbon Receptor. Increase results in improvement of Lupus. Likely many other autoimmune conditions and GDD as well.

I have recommended for several years that both I, and everyone else interested in GDD, should pay attention to research in COVID, COVID vaccine, and autoimmune disease to gain insight into treatment methods that should also assist with GDD.

For years my theory with GDD is that it represents an immune dysregulation primarily involving tissue resident memory T cells. By extension treatments that address T cell dysregulation should be beneficial for GDD. Since I started this line of thinking research into other conditions theorize similar basis for other disease. So more conditions now experts postulate the role of toxins, often focused on metals, and genetic susceptibility. It may well be that in the future specific toxin causing clinical conditions will be prefixed with the causative entity, so: Gadolinium induced fibromyalgia, gadolinium-induced ALS, gadolinium-induced stiff person disease, Gadolinium-induced systemic fibrosis (instead of NSF), and so on. The benefit to sufferers with gadolinium as the cause, is that it is fundamentally treatable, as Gd can be removed. The only other entity as fundamentally treatable would be with lead as a prefix. This is for the time being, until other entities can be as efficiently removed, with chelation or some other removal process.

All of this is preface to this paper describing the role of Aryl Hydrocarbon Receptor (AHR) present in cells throughout the body. Low AHR levels predispose to the presence of T helper cells that release more pro-inflammatory cytokines as shown in Lupus. Increasing AHR alters the composition of T cells and T suppressor or regulatory cells populate which generate immune dampening cytokines, which decrease inflammation and fibrosis. Perhaps the Holy Grail of treatment for immune mediated inflammatory diseases. So rather than immune system suppression, as most autoimmune treatments involve, and GDD employing our chelation with steroid taper strategy. Increasing AHR does not suppress the immune system. Ofcourse the question is what happens if you increase AHR everywhere, beyond localization to regions of disease.

At any rate, this is the study:

Interferon subverts an AHR–JUN axis to promote CXCL13+T cells in lupus

Calvin Law, et al

Nature 631, 25 July 2021.