According to Dr. Behari, the immunologist who started treating patients with LDN, LDN works so well because auto-immune patients have lowered beta-endorphine levels. Thus by blocking the beta-endorphine receptors during the night it would provoke the body in temporarily producing more beta endorphines.
My feeling is that auto-immune patients really all have some degree of dysbiosis and because of the process of neuro-gastro-enterology, some neurotransmitters are inhibited.
Used as a low dose, Naltrexone is able to block the mu opiod receptor but does not affect the other opiod receptors. In blocking the mu opiod receptor, low dose Naltrexone re-establishes the normal balance between the mu and delta opiod receptors, which is necessary for immune competence. Naloxone (sic) has also been show to increase Th1 and decrease Th2 cytokine production, decrease IL-4 production, and increase IL-2 and interferon gamma levels. In many autoimmune diseases, for instance Gravesí disease, low Th1 levels are related to the proliferation of autoreactive T lymphocytes and the ability to produce autoantibodies.
But I'm still on the fence about LDN. It just seems strange that long term blocking of the beta endorphine receptors doesn't do long term damage.