Host-pathogen Interactions in Guillain-Barré Syndrome

Guillain-Barré syndrome (GBS) is a neurological illness in which patients become rapidly paralyzed and require long-term rehabilitation. At present, it is the world’s most frequent cause of acute ascending paralysis in those countries where poliomyelitis has been eradicated (1). GBS is a post-infectious immune-mediated disease and in the last twenty years much progress has been made in elucidating the immune response to infections and peripheral nerves, the types of infection and the mechanism of nerve damage (2). As a consequence, GBS is regarded a model disease for other post-infectious diseases. The aim of the following paragraphs is to present a comprehensive framework for reading the remaining chapters of this thesis. It will focus on the role of infections, antibodies to neural antigens and the presumed immunological and molecular factors that determine why some individuals may develop GBS after infections whereas most do not. A general introduction about the history and clinical aspects of GBS and related disorders will be presented first. Next, the pathogenesis of GBS will be addressed in more detail. The role of serum anti-neural antibodies in the diagnosis of GBS and other immune-mediated neuropathies will be discussed separately. Central to this thesis is the thought that interactions between patients (the host) and microorganisms (pathogens) contribute to the development of this post-infectious syndrome. At the end of this chapter the outline and aims of the studies described in this thesis will be presented.

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