00:01
Multiple sclerosis affects the CNS and here
we have a image showing the microglia in
the CNS and the infiltration of T lymphocytes
from the blood vessels into the CNS.
00:19
Now normally there is a blood brain barrier, but in
multiple sclerosis and another-- a number of other
conditions, this blood brain barrier can become
compromised and inflammatory cells can enter the CNS.
00:36
Th1 cells will secrete gamma interferon
leading to the activation of macrophages.
00:47
These macrophages can secrete
tumor necrosis factor-α.
00:52
Also Th1 cells can help to
activate cytotoxic T-lymphocytes.
01:00
And again these cytotoxic T-lymphocytes can attack
the myelin sheath of the nerve cells in the CNS.
01:10
Astrocytes which are antigen
presenting cells within the CNS which
can present peptides to Th2 cells
will be involved in this process.
01:21
And the Th2 cells can help B-cells to differentiate
into plasma cells and produce autoantibodies.
01:32
The autoantibodies that are produced include
anti-myelin basic protein, anti-myelin
oligodendrocyte glycoprotein, anti-myelin associated
glycoprotein and anti-proteolipid protein.
01:48
In this magnetic resonance image of the brain,
from a patient with multiple sclerosis, we
can see the typical periventricular demyelination
plaques caused by this autoimmune attack.
02:07
Guillain-Barre syndrome occurs following an
infection with a variety of different organisms.
02:15
For example, Campylobacter.
02:20
The autoantibodies are against
peripheral nerve gangliosides.
02:26
And these are thought to arise
due to molecular mimicry.
02:30
There is an acute inflammatory neuropathy
with symmetrical weakness of the extremities.
02:37
Complement activation
results in neuronal damage.
02:42
And in approximately 25% of patients, there
is a respiratory insufficiency that develops.
02:49
So here you can see an antigen presenting
cell interacting with Th2 cells.
02:55
Those Th2 cells will help activate B-lymphocytes to
develop into plasma cells and produce autoantibodies.
03:04
Those autoantibodies can also then go on and
activate complement, leading to the generation
of the membrane attack complex, consistent of
complement components C5b, C6, C7, C8 and C9.
03:19
And this will cause damage
to the Schwann cells.
03:27
In myasthenia gravis, which is
characterized by muscle weakness and
fatigue, there are autoantibodies
against the acetylcholine receptor.
03:38
There is loss or damage to receptors
which is caused by complement activation.
03:47
The autoantibodies can also block the
binding of acetylcholine to the receptor.