Are there Examples of Such an Immune Mechanism? 237
ABO Incompatibility
In this type of hemolytic disease of newborns, the ABO blood type is incom
patible. This occurs when the mother’s blood type of A, B, or O carries a unique
antigen similar to the Rh antigen (i.e., Kell, Duffy, Kidd, Lutheran, Diego, Xg, P,
Ee, Cc, MNSs) that is not found on the mother’s red blood cell surfaces but is
on the fetus’s red blood cells. This condition is considerably less harmful, very
uncommon, and generally not life threatening [4–6].
It is not difficult to imagine that if a fetus is exposed to neurotoxic chemical(s)
that have killed a significant number of neurons, the “unique antigens” that
have leaked into the maternal circulation could lead the mother to produce
antibodies to these antigens which could enter the fetus’s system and further
damage the fetus’s brain development. Here, there is a perpetual double jeop
ardy for the future offspring! The neural antibodies produced during the first
(or previous) pregnancy can harm the subsequent fetuses of these “exposed”
mothers. In Figure 8.1, we have illustrated the mechanism of this terrible double
whammy – the synthetic chemicals (or occasionally an infection) could kill
certain progenitor neurons that lead to specific types of antigens released from
Release of fetal brain antigens
Early stage fetus
Environmental factors enter
pregnant mother’s circulatory
systems at early stages of
gestation and damage
certain brain progenitor
neurons.
Neuronal antigens from the damaged
neurons leak out into mother’s
circulation and adaptive
immune system develop
antibodies to the fetal
neuronal antigens.
Mother’s lgG enters the
fetal brain and interferes
in the normal development
of fetal brain, resulting in
ASD.
(^123)
- Figure 8.1 Illustration of neuroantigens released from the fetal brain and role of maternal
neuroantibodies that can damage a developing fetal brain and may cause autism spectral
disorder (ASD). (See insert for color representation of this figure.)