International Meeting for Autism Research (London, May 15-17, 2008): IMMUNE RESPONSES TO CENTRAL NERVOUS SYSTEM PROTEINS AND VIRUSES IN INDIVIDUALS WITH AUTISM

IMMUNE RESPONSES TO CENTRAL NERVOUS SYSTEM PROTEINS AND VIRUSES IN INDIVIDUALS WITH AUTISM

Thursday, May 15, 2008: 11:30 AM
Avize-Morangis (Novotel London West)
R. S. Fujinami , Department of Pathology, University of Utah, Salt Lake City, UT
J. E. Libbey , Pathology, University of Utah, Salt Lake City, UT
H. H. Coon , Psychiatry, University of Utah, Salt Lake City, UT
N. J. Kirkman , Pathology, University of Utah, Salt Lake City, UT
T. L. Sweeten , Pathology, University of Utah, Salt Lake City, UT
J. N. Miller , Pathology, University of Utah, Salt Lake City, UT
J. E. Lainhart , Pathology, University of Utah, Salt Lake City, UT
W. M. McMahon , Pathology, University of Utah, Salt Lake City, UT
There have been several reports that viral infections and autoimmune responses to central nervous system (CNS) proteins contribute to the pathogenesis of autism. These stem from the hypothesis that immune responses and/or viral infections early in life could alter the development of the nervous system leading to autism. There has been controversy over the presence of autoantibodies to CNS proteins and viruses in autism. To further investigate this question we have measured autoantibody titers to glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) in 33 sera from children with classic onset, 26 children with regressive onset autism and 25 healthy age- and gender-matched subjects. Antibody titers were measured by enzyme-linked immunosorbent assay (ELISA). We did not find a significant difference between the control, classic autism and regression groups. This was confirmed by Western blot analyses. Similarly we did not find a significant difference in antibody titer to MBP between the different groups, which were also confirmed by Western blot analyses. We conclude that antibodies to MBP that may be present in individuals with autism do not contribute to alterations in myelin within the CNS. We also measured antibodies to measles, mumps and rubella viruses using ELISA. No significant differences in antibody titers to measles, mumps and rubella viruses were found among the groups. In addition, there were no significant differences among the groups for total immunoglobulin (Ig)G or IgM. Interestingly, about 25% of individuals with autism had very low or no antibody to rubella virus. We are further exploring how antibodies to rubella virus could contribute to the pathogenesis of autism in this subset of individuals.