Infections, Toxic Chemicals and Dietary Peptides Binding to Lymphocyte Receptors and Tissue Enzymes are Major Instigators of Autoimmunity in Autism

Abstract

Similar to many complex autoimmune diseases, genetic and environmental factors including diet, infection and xenobiotics playa critical role in thedevelopment of autism. In this study, we postulated that infectious agent antigens such as streptokinase, dietary pep tides (gliadin and casein) and ethyl mercury (xenobiotic) bind to different lymphocyte receptors and tissue enzyme (DPP IV or CD26). We assessed this hypothesis first by measuring IgG, IgM and IgA antibodies against CD26, CD69, streptokinase (SK), gliadin and casein pep tides and against ethyl mercury bound to human serum albumin in patients with autism. A significant percentage of children with autism developed anti-SK, anti-gliadin and casein peptides and anti-ethyl mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69 autoantibodies. These antibodies are synthesized as a result of SK, gliadin, casein and ethyl mercury binding to CD26 and CD69, indicating that they are specific. Immune absorption demonstrated that only specific antigens, like CD26, were capable of significantly reducing serum anti-CD26 levels. However, for direct demonstration of SK, gliadin, casein and ethyl mercury to CD26 or CD69, microtiter wells were coated with CD26 or CD69 alone or in combination with SK, gliadin, casein or ethyl mercury and then reacted with enzyme labeled rabbit anti-CD26 or anti-CD69. Adding these molecules to CD26 or CD69 resulted in 28-86 % inhibition of CD26 or CD69 binding to anti-CD26 or anti-CD69 antibodies. The highest % binding of these antigens or peptides to CD26 or CD69 was attributed to SK and the lowest to casein peptides. We, therefore, propose that bacterial antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules, bind to CD26 or CD69 and induce antibodies against these molecules. In conclusion, this study is apparently the first to demonstrate that dietary peptides, bacterial toxins and xenobiotics bind to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism.

Hyperbaric oxygen therapy may improve symptoms in autistic children

“…When compared to typical children, autistic children make significantly more serum antibodies against gliadin and casein peptides [85], produce more pro-inflammatory cytokines [86], and have an imbalance of CD4 + and CD8 + cells [87]. Furthermore, some patients with autism have mucosal inflammation of the stomach, small intestine and colon characterized by ileo-colonic lymphoid nodular hyperplasia [88].…”

Neurotoxic effects of postnatal thimerosal are mouse strain dependent

“…7,8 A large, retrospective study investigating the association of thimerosal-containing vaccines and neurodevelopmental outcomes in an unselected cohort was inconclusive and called for further research into vulnerability factors. 9 An autoimmune diathesis is described in ASD probands [10][11][12][13][14][15] and their first degree relatives. 16,17 Major histocompatibility complex (MHC) genes regulate risk of mercury-induced autoimmunity in mice.…”

Inhibition of MCP-1 and MIP-2 Chemokines in Murine Trichinellosis: Effect of the Anti-Inflammatory Compound L-Mimosine

“…The modulation of chemokines by mimosine can henceforth affect the outcome of the inflammatory response (44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58)(59)(60), the products of which are also important for initiating tissue repair, by chemoattracting immune cells into a wound site. Our study contributes to a better understanding of the mechanism by which blood cells profoundly affect inflammatory responses in vivo and suggests that the inhibitor ofMCP-1 and MIP-2, L-mimosine, may have its effects on inflammatory conditions produced by parasites.…”