What are antibodies???

F ab sites F c site In B cells, antibodies are bound to the membrane at the F c site. Plasma cells secrete antibodies into the blood.

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 T h 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.

NaturalArtificial 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.