So we’re going to look at each of these
four different types, and I’ll explain to
you exactly what’s involved in these different
types of hypersensitivity reaction.
So Type I - IgE mediated
mast cell degranulation.
So here we have a mast cell, and
on the surface of mast cells are
Fc receptors that are specific for the IgE class of antibody.
This is in fact the high affinity
IgE receptor that’s called FcεR1.
So this will bind IgE antibodies
by the Fc region of the antibody.
That’s why it’s called an Fc receptor.
And we all have mast cells sitting in our
tissues that have IgE on their cell surface.
And it doesn’t cause
any problems at all.
The problem arises, is if an antigen comes in which the
IgE is specific for, and that antigen binds to the IgE.
Because what happens then, is that
the IgE antibodies on the surface
of the mast cell get linked together;
we use the term cross-linked.
And if this substance is a completely innocuous substance,
for example grass pollen, we refer to it as an allergen.
It’s going to generate allergy.
And the consequence of the IgE
antibodies being linked together by the
allergen is that the mast cells release
their granules, they degranulate.
Type II hypersensitivity is cytotoxic
antibodies against cell surface antigen.
So here we have a cell surface, with some antigens present on
the cell surface, and antibodies are bound to those antigens.
Sometimes the antibodies can
be directly toxic to the cell.
However, in most cases, other
components of the immune response are
required in order for these antibodies
to actually damage the cell.
So for example, the classical pathway of complement may become
activated, leading to the production
of the membrane attack complex.
Or killer cells, that is any cell
that is able to participate in ADCC.
So this term K-cell is used as a generic
description of cells able to participate in ADCC.
There’s only two things you
need from a cell to do that.
You need it to have an Fc receptor, and you need
it to be able to produce toxic molecules.
Or macrophages that again have Fc receptors on their
surface and are able to attack the coated cell.
Type III hypersensitivity is immune
complex mediated hypersensitivity.
Now, all that term means, immune
complex, is simply an antibody bound
to an antigen, and you know that’s what antibodies do isn’t it?
They bind to antigens.
But in this situation, there is a binding to
an inappropriate antigen or immune complexes
are becoming trapped in small tissue
spaces in the body and causing pathology.
So for example, macrophages can become
activated, complement can become activated.
There will be recruitment of neutrophils if
complement component C5a is generated, because
that’s a very potent chemotactic factor for
neutrophils, and pathology will ensue.
And then finally, Type IV hypersensitivity,
delayed type hypersensitivity.
It’s called delayed type hypersensitivity
because it takes a little while to get going.
The other three types, you can have
antibody that's already present, and as soon
as the antigen comes into the body,
the response will happen immediately.
For T-cells, you need them to expand up in number, to
proliferate, to differentiate, and to start secreting cytokines.
So typically, type IV hypersensitivity takes two
or three days before you actually see any effects.
And there is recognition of peptide MHC Class II
by the T-cell receptor on a T-cell that is going to
mediate this hypersensitivity reaction, most commonly
by producing excessive amounts of cytokines.