00:01
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.
00:11
So Type I - IgE mediated
mast cell degranulation.
00:16
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.
00:26
This is in fact the high affinity
IgE receptor that’s called FcεR1.
00:34
So this will bind IgE antibodies
by the Fc region of the antibody.
00:39
That’s why it’s called an Fc receptor.
00:42
And we all have mast cells sitting in our
tissues that have IgE on their cell surface.
00:48
And it doesn’t cause
any problems at all.
00:50
The problem arises, is if an antigen comes in which the
IgE is specific for, and that antigen binds to the IgE.
01:02
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.
01:10
And if this substance is a completely innocuous substance,
for example grass pollen, we refer to it as an allergen.
01:19
It’s going to generate allergy.
01:24
And the consequence of the IgE
antibodies being linked together by the
allergen is that the mast cells release
their granules, they degranulate.
01:42
Type II hypersensitivity is cytotoxic
antibodies against cell surface antigen.
01:50
So here we have a cell surface, with some antigens present on
the cell surface, and antibodies are bound to those antigens.
01:59
Sometimes the antibodies can
be directly toxic to the cell.
02:05
However, in most cases, other
components of the immune response are
required in order for these antibodies
to actually damage the cell.
02:15
So for example, the classical pathway of complement may become
activated, leading to the production
of the membrane attack complex.
02:25
Or killer cells, that is any cell
that is able to participate in ADCC.
02:32
So this term K-cell is used as a generic
description of cells able to participate in ADCC.
02:40
There’s only two things you
need from a cell to do that.
02:43
You need it to have an Fc receptor, and you need
it to be able to produce toxic molecules.
02:50
Or macrophages that again have Fc receptors on their
surface and are able to attack the coated cell.
03:07
Type III hypersensitivity is immune
complex mediated hypersensitivity.
03:12
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.
03:21
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.
03:33
So for example, macrophages can become
activated, complement can become activated.
03:40
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.
03:53
And then finally, Type IV hypersensitivity,
delayed type hypersensitivity.
03:58
It’s called delayed type hypersensitivity
because it takes a little while to get going.
04:02
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.
04:10
For T-cells, you need them to expand up in number, to
proliferate, to differentiate, and to start secreting cytokines.
04:18
So typically, type IV hypersensitivity takes two
or three days before you actually see any effects.
04:26
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.