When we are very young, our immune
system is not fully developed.
So immaturity can also be a cause
of secondary immunodeficiency.
Neonates have a relatively immature immune
system, particularly if delivered pre-term.
There is susceptibility to infection and this
correlates with the degree of prematurity.
Both T-cells and B-cells in the neonate are
naïve, they haven’t encountered antigen yet.
And therefore they respond
relatively slowly to infection.
In some infants there is a transient
hypogammaglobulinemia of infancy in which IgG
levels remain low following catabolism
of placentally-transferred maternal IgG.
This is usually asymptomatic.
Maternal IgG is transported across the placenta
by the neonatal IgG-Fc receptor (FcRn).
So antibodies from the mother are
picked up by FcRn and transferred
across the placenta, and released into the fetal circulation.
The newborn therefore contains the same
antibody specificities as the mother because
the antibody is coming from the mother
rather than being produced by the fetus.
In immaturity, maternal IgA and IgG in breast
milk is particularly important for the newborn.
Ingested secretory IgA protects the newborn
against microbial colonization in the gut.
Whilst ingested IgG antibodies are transported into the
infant’s circulation by the FcRn on gut epithelium.
Here we can see the serum immunoglobulin levels
in the newborn as a percent of adult values.
Our own B-cells are beginning to
make IgM antibodies before we’re
born, but only very small levels
are produced by the time of birth.
But within the months following birth, IgM levels within a
year or so reach the level that you would find in the adult.
IgG follows a little bit later on,
remember IgM is characteristic of
the primary immune response and IgG
of the secondary immune response.
And at the time of birth, there
is very little IgG in the infant’s
circulation that is being produced
by the infant’s own B-lymphocytes.
They’re just reaching the stage of maturity
when they can begin to make antibody.
IgA levels are also vanishingly small at the
time of birth but will increase over time.
However, with respect to IgG, there is in fact quite a lot
of IgG in the fetal circulation and in the newborn circulation.
And that’s because IgG is transferred across
the placenta as we’ve just seen using the FcRn.
This maternally derived antibody will begin to
be catabolised once the newborn has been born.
And IgG has a half life of
around about three weeks.
So three weeks after birth, half of the
maternal antibody will have been catabolised.
Six weeks after birth, there’ll only
be 25% of the maternal antibody.
But the infant is now beginning to make their own IgG, so
there will be a dip in the level as the maternal IgG is
catabolised, but then the infant’s own IgG will come up and
eventually there will be a rise in the overall IgG level.
Pregnancy is a condition in which
there is a natural immunosuppression.
This occurs in order to avoid rejection
of the semi-allogeneic fetus.
Remember, half of the genes in the fetus,
will have come from the male partner.
Immunosuppression is largely focused at the
maternal-fetal interface in the placenta, to stop an
immunological rejection of this semi-allogeneic
fetus where half of the genes are from the dad.
However, there is some degree of systemic
suppression of the immune response.
And pregnant women have a degree of increased
incidence and severity of infection.
There is no evidence of risk of vaccinating
pregnant women with inactivated virus
or bacterial vaccines or with toxoids,
which are inactivated bacterial toxins.
However, live virus vaccines are contraindicated because of the
theoretical risk of transmission of live virus to the fetus.