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Transcript
A newborn mammal has no opportunity to develop protective
antibodies on its own, unless, as happens very rarely, it was
infected while in the uterus.
Yet it is born into an environment similar to its mother's, which
contains all the potential microbial invaders to which she is
exposed.
Although the fetus possesses the components of innate
immunity, it has few or none of its mother's lymphocytes.
The placenta generally prevents the maternal lymphocytes from
crossing into the uterus, where they would recognize the fetal
tissues as foreign antigens and cause a reaction similar to the
rejection of an incompatible organ transplant.
What is transferred across the placenta in many species is a fair
sample of the mother's antibodies. How this happens depends on
the structure of the placenta, which varies among species.
In humans maternal IgG antibodies—but not those of the other
immunoglobulin classes—are transported across the placenta
into the fetal bloodstream throughout the second two-thirds of
pregnancy. In many rodents a similar transfer occurs, but
primarily across the yolk sac.
Maternal immunity,
Passive immunity Immunity in a neonate provided by IgG
antibodies from the mother passing across the placenta to the
fetus; MI is immunoprotective for up to 6 month .
Maternal antibody,
an antibody transmitted from mother to fetus via the placenta.
Such antibodies can provide immunity for the fetus and the
newborn for up to 6 months after birth.
They may also cause hemolytic anemia in newborns in cases of
Rh or ABO blood group incompatibility between mother and
child.
Human colostrum is also rich in IgA, with the concentration
highest immediately after birth.
After a newborn has received its supply of maternal antibodies, it
is as fully protected as its mother. This means, of course, that if
the mother has not developed immunity to a particular pathogen,
the newborn will likewise be unprotected.
For this reason, a physician may recommend that a prospective
mother receive immunizations against tetanus and certain other
disorders. (The active immunization of pregnant women against
certain viral diseases, such as rubella [German measles], must be
avoided, however, because the immunizing agent can cross the
placenta and produce severe fetal complications.)
As important as the passively transferred maternal antibodies
are, their effects are only temporary. The maternal antibodies in
the blood become diluted as the animal grows; moreover, they
gradually succumb to normal metabolic breakdown.
Because the active development of acquired immunity is a slow
and gradual process, young mammals actually become more
susceptible to infection during their early stages of growth than
they are immediately after birth.
Occasionally the transfer of maternal antibodies during fetal life
can have harmful consequences. A well-known example of this
is erythroblastosis fetalis, or hemolytic disease of the newborn, a
disorder in which maternal antibodies destroy the child's red
blood cells during late pregnancy and shortly after birth. The
most severe form of erythroblastosis fetalis is Rh hemolytic
disease, which develops when:
The fetus is Rh-positive; that is, its red blood cells carry an
antigen known as the Rh factor.
The mother is Rh-negative, which is to say her red blood cells
lack the Rh factor.
The mother's immune system has been previously activated
against the Rh antigen; this usually is the result of exposure to
fetal cells during the birth of an earlier Rh-positive baby or a
transfusion of Rh-positive blood.
Rh hemolytic disease can be prevented by giving the mother
injections of anti-Rh antibody shortly after the birth of an Rhpositive child. This antibody destroys any Rh-positive fetal cells
in the maternal circulation, thereby preventing the activation of
the mother's immune system should she conceive another Rhpositive fetus.
In addition to their importance in cooperating with B cells that
secrete specific antibodies, T cells have important, separate roles
in protecting against antigens that have escaped or bypassed
antibody defenses.
Immunologists have long recognized that antibodies do not
necessarily protect against viral infections, because many viruses
can spread directly from cell to cell and thus avoid encountering
antibodies in the bloodstream.
One major change that occurs as the body ages is a process
termed "thymic involution." The thymus, located above the heart
behind the breast bone, is the organ where T cells mature.
Age-related changes in cell mediated immunity :1- As humans age, the thymus naturally atrophies. The volume
of thymic tissue in a 60-year-old adult is less that 5% that of a
newborn, and it is postulated that if humans lived to be more
than 120, the thymus would disappear altogether. Although T
cells are produced continuously throughout life, over time this
progressive decay of the thymus causes a sharp decrease in the
number and type of T cells produced. It is not known why the
thymus deteriorates in this fashion.
2- A marked difference has been observed between young and
old subjects in the subpopulations of naive and memory T cells.
In newborns, the ratio of naive to memory T cells is quite high;
in adults the ratio is reversed because most of the naive T cells
have been exposed to antigen, and hence converted to memory
cells. The elderly have almost no naive T cells at all, since as the
thymus progressively deteriorates with age, fewer T cells are
produced, and the naive T cell subpopulation is not replenished.
3- Another defect of T cell activation among the elderly is
characterized by a decrease in calcium. Calcium is a vital
element that is absolutely crucial for many biochemical
reactions, including signal transduction.
4- Decreased amounts of calcium can also inhibit production of
cytokines, proteins responsible for coordinating the interaction
with antigen and amplifying the immune response.
5- Age-related genetic alterations occur within T cells as well.
References :,Updated March 1999 , The Immunology of AgingDeborah B. Whitman
2012 Encyclopædia Britannica
http://www.britannica.com/nobelprize/article-215587
Mosby's Medical Dictionary, 8th edition.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by
The McGraw-Hill Companies