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.
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.
Th1 cells will secrete gamma interferon
leading to the activation of macrophages.
These macrophages can secrete
tumor necrosis factor-α.
Also Th1 cells can help to
activate cytotoxic T-lymphocytes.
And again these cytotoxic T-lymphocytes can attack
the myelin sheath of the nerve cells in the CNS.
Astrocytes which are antigen
presenting cells within the CNS which
can present peptides to Th2 cells
will be involved in this process.
And the Th2 cells can help B-cells to differentiate
into plasma cells and produce autoantibodies.
The autoantibodies that are produced include
anti-myelin basic protein, anti-myelin
oligodendrocyte glycoprotein, anti-myelin associated
glycoprotein and anti-proteolipid protein.
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.
Guillain-Barre syndrome occurs following an
infection with a variety of different organisms.
For example, Campylobacter.
The autoantibodies are against
peripheral nerve gangliosides.
And these are thought to arise
due to molecular mimicry.
There is an acute inflammatory neuropathy
with symmetrical weakness of the extremities.
results in neuronal damage.
And in approximately 25% of patients, there
is a respiratory insufficiency that develops.
So here you can see an antigen presenting
cell interacting with Th2 cells.
Those Th2 cells will help activate B-lymphocytes to
develop into plasma cells and produce autoantibodies.
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.
And this will cause damage
to the Schwann cells.
In myasthenia gravis, which is
characterized by muscle weakness and
fatigue, there are autoantibodies
against the acetylcholine receptor.
There is loss or damage to receptors
which is caused by complement activation.
The autoantibodies can also block the
binding of acetylcholine to the receptor.