Is There a Link between Autoimmunity and Other Forms of Neurodevelopmental 249contribute towards ASD, is a highly specific phenomenon and cannot be gen
eralized to other autoimmune diseases where a mother is suffering from an
autoimmune disorder(s). In the case of any autoimmune disease, a mother
suffers from a breakdown of the normal immune system and develops anti
bodies to a “specific” antigen or antigens of her own tissue. These disorders
originate from the mother’s own body and not from a fetus (which we
described above in detail). For example, in the case of autoimmune hemolytic
anemia, a mother forms antibodies to Rh I antigen found on her own red
blood cells. This should not be confused with erythroblastosis fetalis, where
the problem arises from the incompatible fetus (i.e., Rh+ red blood cells).
It would be ridiculous to claim that all mothers who were exposed to Rh+ red
blood cells from their fetuses would have ASD children! Similarly, in another
example, in the case of acute rheumatoid arthritis, the mother forms antibod
ies to a common bacterial agent, Streptococcus. Antibodies formed to this
pathogen can result in arthritis (inflammation of joints), myocarditis (inflam
mation of heart tissues), and sometimes inflammation of heart valves. In the
majority of cases, the autoantibodies a mother forms are directed to her own
body and may not have any effect on the developing fetus in her womb.
However, we believe that in some cases and in some forms of autoimmune
disorders, the mother can form antibodies to a wide range of antigens in her
own body that have the potential to cross the placenta and reach a developing
fetus. A prime example of such an unusual illness is systemic lupus erythema
tosus (SLE). In this case, a SLE patient develops antibodies to DNA, histones,
ribosomes, small nuclear ribosomal nuclear proteins, and a large array of
other tissue antigens. If the maternal IgG autoantibodies cross the placenta,
they may harm the fetus.
Keeping the above limitations in mind and that all mothers suffering from
autoimmune disorders would not give birth to ASD offspring, a large study by
Vinet et al. [25] evaluated whether children born to mothers with SLE would
have an increased risk of ASD compared with children born to mothers with
out SLE. Their study population included 719 children born to 509 SLE
women and 8,493 children born to 5,824 control women. Children born to
women with SLE more frequently had a diagnosis of ASD compared with con
trols. The difference between the SLE and control groups was 0.8%. In conclu
sion, compared with children from the general population, children born to
SLE women had an increased risk of ASD, although, in real life, it represents a
rare event. If should also be noted that SLE individuals are clinically different
than typical individuals. A study by Tiosano et al. (26) analyzed 5,018 indi
viduals with SLE and 25,090 matching controls for schizophrenia in Israel.
They found a positive association between SLE and schizophrenia across
patients of different age, gender, and social economic status. This association
may provide additional insight into our understanding of the pathophysiology
of the two disorders.