The author hypothesized that MS is a humoral autoimmune disease (mediated by auto-antibodies), caused by faulty interplay between myelin-specific, dimeric IgE, specifically competing non-IgE antibodies and IgE-triggered degranulating mast cells.
IgE is a type of antibody linked with allergic diseases.
Mast cells are a type of white blood cell that mediate allergic reactions.
The principal fault was believed to be insufficient quantity of protective, specific non-IgE antibodies. Also conjectured was the possibility of an unexpected and adverse immune suppression caused by none-MS pharmaceuticals being consumed by patients for their MS or for other conditions. To test both hypotheses, a mimotopic, peptide antigen-based, serum immunoassay was developed to measure dimer-bound IgE excess among MSers, wherein the IgE specifically complexes with two or more myelin surface epitopes at an interval of 40-100 Angstroms, a separation critical for mast cell degranulation and cell damaging effect. MS test sensitivity and specificity, when analyzing five previously untreated patients for dimeric IgE presence, was 100%. In direct comparison, twenty age- and gender-matched female and male control subjects were test negative. Analysis of 35 MSers, who were concomitantly being treated with potentially immunosuppressive pharmaceuticals, appeared to show the substances’ negative effect upon MS causation, progression, or specific immunoassay performance. Therefore, MS is likely an autoimmune disease caused by IgE-mediated mast cell degranulation possibly in conjunction with immunosuppressive agents.
“This work suggests MS is an autoimmune disease with a problem of immunoglobulin E, which is usually associated with allergies and asthma. I wonder what Enteron Inc is engaged with? Dealing with the problem of Myelin-specific IgE? This work will clearly need to be reproduced. It is my experience that MSers have a reduced amount of allergic disease. I am not convinced by these results.”