Third Line of Defense Part II*B cells and antibodies

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What are antibodies???
Fab sites
In B cells, antibodies
are bound to the
membrane at the Fc
site. Plasma cells
secrete antibodies into
the blood.
Fc site
IgD:
IgM:
IgA:
The bad news: antibody/antigen
complexes that are not eliminated can
obstruct capillaries or collect in joints
(serum sickness)
Complement (review: a cascade of proteins in
the Second Line of Defense)
Complement can be activated by antibodies that
have bound to antigen (IgM and IgG only). This
increases the chances that they will lyse the
cell. Usually bacteria are killed this way.
When antibodies bind to non-self antigens,
they change surface charges on the antigens,
which makes them more likely to be attacked
by phagocytes. This process of making the
antigen more “attractive” to phagocytosis is
called opsonization.
First exposure to antigen: Sensitizing dose.

Latent phase: no antibody titer at first.
This is when antigen is recognized by
antibodies on the surface of B cells, the B
cells differentiate into plasma cells by
interaction with Th cells.

Primary response: First antibody to rise in
titer is IgM. Titer rises, then falls (2-4
weeks). This rise in IgM titer is followed by
a similar rise in IgG titer (delayed by a week
or two). The IgG titer falls somewhat, but
remains elevated long after the primary
response ends.
Clinically, the patient is having the expected
reaction to the pathogen. Depending on the
portal of entry, the rise in IgG may also be a
rise in IgA or even IgE (if it’s an allergen)

Secondary response: The second exposure
to antigen (sometimes called the “shocking
dose”), causes an immediate and rapid
increase in IgG titer. There is also a slight
increase in IgM. Antibody responses
(neutralization, opsonization, or
complement fixation) are rapid and
thorough.
Clinically, with an effective antibody
response, the patient is unaware that
anything has happened.
Natural
Artificial
Active
Passive
• Natural: occurs without man-made intervention
• Artificial: medical science has induced the immunity.
• Active: the patient mounts his/her own immune response
• Passive: the patient receives immune cells or antibodies (s)he has not
produced.

Edward Jenner—1796. Determined
that injecting people with serum from
cowpox (a minor skin irritation) made
them immune to smallpox (a
devastating fatal disease).

Vaccination: creating an antibody
response by sensitizing the patient to
antigens of a pathogen without
exposing them to the pathogen itself.



Pieces of antigens (toxoids)
Dead pathogens (Salk polio vaccine,
influenze)
Live attenuated (non-virulent) pathogens
(Sabin polio vaccine)
Live viruses are often maintained in raw
eggs.
MYTH
BUSTED!!!!!
Because antibodies are specific to given
pathogens, they can be used as a diagnostic
tool.

Antibodies can be complexed to latex
particles in suspension. This allows
identification of antigens in many clinical
specimens (e.g. Staph aureus, C.diff,
meningitis organisms, tuberculosis). This
is a way to eliminate the need for culture if
there is no time.

Blood banking: anti-A, anti-B, anti-Rh,
crossmatching.

Antibody testing can be against bacterial
capsules, flagellae, or fimbriae (Salmonella)

Can create antibodies against other antibodies!
We create antibodies to human IgG in rabbits
(HIV test)

Antibodies can be “tagged” with radioactive
isotopes, fluorescent compounds, or colored
enzymatic compounds (RIA, ELISA) to allow
rapid and extremely sensitive detection of
antigens.
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