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Multiple Sclerosis
Lindsay Nicholson, University of Bristol, UK
© The copyright for this work resides with the author
Multiple sclerosis (MS) is a human disease that affects the nervous
system. The most common pattern of disease is intermittent attacks
affecting sight, mobility or sensation followed by gradual recovery.
Over time the attacks can lead to permanent disability. The most
widely accepted explanation for MS is that the immune system
orchestrates repeated episodes of inflammation within the brain,
because its normal ability to distinguish healthy tissue from infected
tissue has failed. With modern imaging techniques such as magnetic
resonance imaging (MRI), these events within the brain can be
visualised. As the disease progresses inflammation cause scars,
which are associated with loss of insulation on the nerve and with
secondary loss of nerve cells. These are recognised at post mortem
as ‘sclerosis’.
As discussed (See: Autoimmunity: introduction), genetic,
environmental and stochastic elements all contribute to the
development of disease, and while treatment for MS has advanced
rapidly in recent years, with the powerful new drugs in development
showing a great deal of efficacy in slowing the rate of MS attacks,
these drugs also have rare but extremely serious side effects, and
further advancements in treatment are needed.
So what are the pressing questions about the immunology of MS that
researchers need to answer? Some core concerns are: why does
normal immune regulation fail, why does the disease remit and
relapse, and how can we move treatment towards the goal of
selectively shutting down the anti-self response while preserving the
immune system’s ability to deal with infection?
Figure 1. In multiple sclerosis, loss
of insulation on the nerve and
secondary loss of nerve cells arises
in the context of inflammation driven
by immune cells that target proteins
in the brain.
Most people agree that MS is triggered by an external event, and this is certainly the case in
animal models that are used to study this condition. However, it is unlikely that acute infection with
a single microorganism provides a unique initiation point. And it is important to recognise that
animal models show that autoimmunity can be spontaneous and sometimes becomes commoner
where rates of infection are low rather than high. It is extremely challenging to devise ways of
studying this trigger in humans and most of our understanding of this process comes from animal
Relapses and remission are likely to be related to activation of cell traffic into the central nervous
system triggered by perturbation of the immune response. They do correlate, in animal models,
with a spreading of the immune response to different brain proteins but this may simply reflect
ongoing inflammation. Other models show that periodic behaviour can arise spontaneously, when
the target of the immune response cannot be eliminated. It is also possible that relapses are
triggered more easily than the first attack and so happen more often.
Because new drug treatments have rare but extremely serious side effects, we need to learn how
to predict those patients with the worst prognosis and offer them these treatments early, while
holding them back when progression is expected to be slow. This is another ambitious goal that
the research of the future will address.
Finally selective immune therapy remains an important focus and a real possibility. Using
vaccination to teach the immune system to ‘remember’ an infection before it is encountered, is one
of the great triumphs of clinical immunology and public health of the 20th century. What the
treatment of autoimmunity requires in the 21st century is teaching the immune system to forget.