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Bacterial Infects and Milk Antigens May Modulate Autism Autoimmune Responses



Buku Bunga Rampai


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09/24/2002


Reprinted of abstracts by permission of National Library of Medicine http://www.ncbi.nlm.nih.gov

Vojdani A, Campbell A, Anyanwu E, Kashanian A, Bock K, Vojdani E.Section of Neuroimmunology, Immunosciences Laboratory, Inc., 8693 Wilshire Boulevard, Suite 200, 90211, Beverly Hills, CA, USA

We measured autoantibodies against nine different neuron-specific antigens and three cross-reactive peptides in the sera of autistic subjects and healthy controls by means of enzyme-linked immunosorbent assay (ELISA) testing.

The antigens were myelin basic protein (MBP), myelin-associated glycoprotein (MAG), ganglioside (GM(1)), sulfatide (SULF), chondroitin sulfate (CONSO(4)), myelin oligodendrocyte glycoprotein (MOG),
alpha,beta-crystallin (alpha,beta-CRYS), neurofilament proteins (NAFP), tubulin and three cross-reactive peptides, Chlamydia pneumoniae (CPP), streptococcal M protein (STM6P) and milk butyrophilin (BTN).

Autistic children showed the highest levels of IgG, IgM and IgA antibodies against all neurologic antigens as well as the three cross-reactive peptides.

These antibodies are specific because immune absorption demonstrated that only neuron-specific antigens or their cross-reactive epitopes could significantly reduce antibody levels.

These antibodies may have been synthesized as a result of an alteration in the blood-brain barrier. This barrier promotes access of preexisting T-cells and central nervous system antigens to immunocompetent cells, which may start a vicious cycle.

These results suggest a mechanism by which bacterial infections and milk antigens may modulate autoimmune responses in autism.

PMID: 12161033 [PubMed - in process]


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