ABSTRACT
Serum antibodies in 100 mothers of children with autistic disorder (MCAD) were compared to 100 age-matched mothers with unaffected children (MUC) using as antigenic substrates human and rodent fetal and adult brain tissues, GFAP, and MBP. MCAD had significantly more individuals with Western immunoblot bands at 36 kDa in human fetal and rodent embryonic brain tissue. The density of bands was greater in fetal brain at 61 kDa. MCAD plus developmental regression had greater reactivity against human fetal brain at 36 and 39 kDa. Data support a possible complex association between genetic/metabolic/environmental factors and the placental transfer of maternal antibodies in autism.
Subject(s)
Autistic Disorder/immunology , Brain/immunology , Immunoglobulin G/blood , Isoantibodies/blood , Isoantigens/immunology , Nerve Tissue Proteins/immunology , Adult , Aged , Animals , Antibodies, Heterophile/blood , Antibodies, Heterophile/immunology , Autoantibodies/blood , Autoantibodies/immunology , Birth Order , Brain/cytology , Brain/embryology , Brain-Derived Neurotrophic Factor/blood , Female , Glial Fibrillary Acidic Protein/immunology , Humans , Immunoglobulin G/immunology , Isoantibodies/immunology , Male , Maternal-Fetal Exchange , Middle Aged , Mothers , Myelin Basic Protein/immunology , Neurons/immunology , Parity , Pregnancy , Rats , Species SpecificityABSTRACT
The study examined whether maternal serum antibodies from mothers of autistic children preferentially bind to lymphocytes of their autistic children compared with unaffected siblings. In a previous study, maternal serum antibodies from mothers mediated cytotoxicity with complement to lymphocytes of their autistic children. Here, maternal serum antibody binding was examined by flow cytometry. We compared levels of mothers' serum binding against peripheral blood monocytes of their autistic children vs unaffected siblings. Because the level of binding to peripheral blood monocytes could be low, binding was examined in specific lymphocyte subpopulations. In 19 samples, the mean level of maternal serum immunoglobulin G binding to CD4 and CD8 T cells, B cells, natural killer cells, and macrophages was not significantly different from the mean level of binding to unaffected siblings. The percentages of different subpopulations were not significantly different between autistic children and unaffected siblings, although a trend (P < 0.1) emerged, i.e., autistic children displayed a higher percentage of natural killer cells and a lower percentage of B cells. These findings cast doubt on a direct effect of maternal antibodies, but do not preclude potential intrauterine pathogenic immune mechanisms in autism.