of bacteria and bacterial toxins
"Antibody dependant cellular cytotoxicity" or "ADCC"
is the classic method for the immune system to destroy invading
bacterial pathogens and anything else it believes is alien and
dangerous. Antibodies produced against an antigen will bind to
their target. Ultimately enough antibodies will bind to virtually
coat the bacteria and this coating is incredibly stimulating to
immune system cells if the dominant antibody is IgG. The bacterial
target for destruction is said to be "opsonized". Opsonizing
a target with IgG is a red flag for cells with cytotoxic destructive
ability. Some T cytotoxic cells and Natural Killer cells have
cell surface receptors for the Fc portion of an antibody. If several
Fc receptors bind to antibodies coating a bacteria cell surface
this cross linking activates the cell to carry out cytotoxic destruction
as we described before. Antibody coating is also a flag to phagocytes
which also have Fc receptors on their surface. If the opsonized
target is small enough a phagocyte will bind to the antibody coating
and engulf the entire particle to break it down. There are other
methods of Tc cell and phagocytic recognition of antigens that
don't require antibody opsonization (described later).
Some bacteria are motile, they have propellers to move them
around and spread their infection. The protein propellers look
like corkscrews which are attached within the bacterium to an
organic motor. Some bacteria have several propellers to more them
around. Antibodies can prevent the movement of these types of
bacteria and so slow down the spread of infection by cross linking
the propellers and preventing them from rotating. The equivalent
of a boat getting a fishing net wound around its propeller.
Antibodies may also bind together several bacteria into an immune
complex. Linking the bacteria together also limits their ability
to move and function properly. The large size of the immune complex
also makes it easier for phagocytic cells to latch onto it and
engulf the bacteria.
Bacterial toxins are waste products produced in bacterial respiration.
Different bacteria produce different waste products. Some may
be harmless to us but others are highly toxic chemicals. These
molecules can be neutralized by a coating of antibody. The antibody
coat physically stops a toxic molecule from coming into contact
with cells of the body. The coating also promotes uptake by phagocytes
and break down of the dangerous molecules.
Viruses are unable to replicate without the use of host cells.
Viruses must invade a cell and hijack its machinery to produce copies
of the virus which are then released from the cell to infect other
cells. Any virus infected cell will express viral proteins on its
So there are two points at which antibody can work to neutralize
a virus. They can coat a virus while it is free floating and looking
for a cell to invade or they can coat a virus infected cell by binding
to viral markers on the cell surface. Coating a cell will flag it
for cytotoxic destruction. Coating a virus particle will both flag
it for phagocytosis and it will stop the virus from binding and
then invading a cell.
protection of embryos / newborns
Clearly during embryonic development of a baby there is a window
of opportunity for pathogens to invade without much resistance from
an underdeveloped immune system. While the embryo's immune functions
are developing it is the job of the mother's immune system to protect
the embryo. Physically of course the embryo is protected by the
mothers tissues but internally it must rely on passive transfer
of antibodies from the mother into its own blood stream.
Only IgG type antibodies are able to cross the placenta into the
embryo and this begins from around 2.5 months after fertilization.
The delay is in part the time it takes for the egg to bury in the
womb wall and for the placenta to develop. The embryo's ability
to produce antibody is very poor. IgM starts to be produced from
around 4.5 months but remains well below half the production rate
an adult has. Production of other antibody types does not begin
until after birth.
Maternal IgG concentration in the embryo's blood stream rises
at a rapid rate until birth. At birth, with the loss of the placental
connection, the IgG concentration of the newborn tails off over
the next nine months or so. Almost immediately from birth IgA and
IgG type antibodies begin to be produced but it takes time for their
concentrations to reach adult levels. Even when a child is one year
old IgG is only 60% of an adult's concentration, IgM 75% and IgA
20%. This leaves the child relatively more exposed to pathogens
and more susceptible to infection. To help reduce risk IgG antibodies
can be supplied to the child by breast feeding. Maternal milk contains
IgG antibody and the baby can absorb this through the gut.
cell activation through IgD and / or IgM receptors
IgD and IgM is spread out over the entire surface of each and
every B cell. It is possible for B cells to have the other antibody
types, IgG, IgA and IgE, expressed on their cell surface but this
is a rare occurrence and only happens on B cells in certain specific
areas of the body. For example B cells in the walls of the intestines
express IgA on their surface.
The Fc portion of each antibody is rooted in the cell membrane
leaving the branches of the "Y" shape exposed. This positioning
allows the antibody binding sites to be unobstructed by other cell
surface receptors neighboring the antibody.