Let's imagine for a minute that you found yourself in the somewhat unfavorable position of having being bitten by a venomous snake.
Now, to treat that, you might get injected with anti-venom, which is the serum, or just the liquid part of blood and it’s had the coagulation proteins removed, and it comes from another animal, like a mouse, and that mouse has already encountered that particular venom and so it’s developed antibodies against it.
These antibodies can bind to the venom molecules and render them harmless.
It’s just like attacking a friendly police officer that’s trying to help you out.
Serum sickness is a type III hypersensitivity reaction, which means that it’s mediated by immune complexes, which are combinations of antibodies and soluble antigens, in this case the antigens are the foreign antibodies in the serum.
B cells have multiple IgM antibodies on their surface and they act like receptors.
When an antigen binds to two of these receptors it’s called cross-linking.
Nearby T helper cells can then bind to the MHC class II protein via their T cell receptor, this happens along with costimulatory molecule CD4.
This means that it changes from producing IgM antibodies to producing IgG antibodies instead.
After class switching, B cells become plasma cells and they focus on producing large amounts of this IgG antibody.
The IgG antibodies bind to the antigen on pathogens like a bacterium the IgG antibodies would bind to the antigen on the bacterium and mark it for destruction by macrophages and neutrophils.
In serum sickness, however, plasma cells start producing IgG antibodies in response to the antibodies in foreign serum that gets mistaken for a harmful antigen.