I came across a reference to "functional autoantibodies" in autoimmune diseases, and started going down rabbit holes on the web to see if I could find out more. I came across this paper which mentioned hypothyroidism and hyperthyroidism in the abstract.
Title : As per this post
Link : sciencedirect.com/science/a...
Abstract
The recent detection of stimulatory autoantibodies as a characteristic feature of systemic sclerosis (scleroderma), established the presence of such autoantibodies as a characteristic pathophysiologic finding in a second classical autoimmune disease after autoimmune thyroid disease. This observation raises the possibility of a new paradigm in abnormal autoimmune function, the presence of stimulatory (and suppressive), functional autoantibodies as characteristic features of abnormal autoimmune function. The assumption of such a paradigm opens interesting new research avenues within rheumatology and in other medical specialty areas. Within reproductive medicine, and akin to the concept of hypo- and hyperthyroidism, the possible juxtaposition of polycystic ovarian syndrome (PCOS) and premature ovarian aging (POA), as opposite abnormalities of adrenal function, under control of autoimmune adrenal antibodies, deserves further investigation.
There is more information on this paper at the above link but it is not a complete reproduction of the paper, it is just some snippets.
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Having found the above, I went and looked for info on "What are functional autoantibodies" and, frankly, didn't find much I could understand. But I found this which suggests that functional autoantibodies are relevant to lots of common conditions, including a few which sometimes get mentioned on the forum.
Title : Functional autoantibody diseases: Basics and treatment related to cardiomyopathies
Link : imrpress.com/journal/FBL/24...
Abstract
In the 1970s, autoantibodies directed against G-protein-coupled receptors (GPCR, GPCR-AAB) were discovered. After receptor binding, GPCR-AAB trigger uncontrolled receptor mediated signal cascades, thus producing pathologies. Diseases associated with such functionally active autoantibody type (functional autoantibodies) can be called “functional autoantibody diseases”. Here we focus exclusively on GPCR-AAB directed against the GPCR’s extracellular loops. The GPCR’s role in the pathogenesis and progression is accepted in idiopathic dilated cardiomyopathy and is increasingly considered in diseases such as Chagas’ cardiomyopathy, peripartum cardiomyopathy, hypertension, diabetes mellitus and scleroderma and even dementia, complex regional pain syndrome and postural orthostatic tachycardia syndrome. We briefly summarize the mechanistic background of GPCR-AAB induced pathologies, mainly focused on autoantibodies targeting the β1-adrenergic and muscarinic 2 receptors, due to their importance for cardiomyopathies. Furthermore, treatment strategies for “functional autoantibody diseases”, such as for GPCR-AAB removal (therapeutic plasma exchange, immunoadsorption) and in vivo GPCR-AAB attack (intravenous IgG treatment, B-cell depletion, GPCR-AAB in vivo binding and neutralization) are critically reflected with respect to their patient benefits focused on but not exclusive to patients with dilated cardiomyopathy.
The above paper can be freely downloaded.
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