Abstract
Until recently the peripheral nervous system (PNS) was thought to be one of the immune privileged sites, where no immune reaction can take place (Streilein, 1995). Thus this sensitive tissue could be protected from immune-mediated destruction. In the meantime it has become clear that cells of the immune system can cross the blood-nerve-barrier causing inflammation and damage of the nerve fibres and glial cells. When activated autoreactive T-cells enter the nervous system they can destroy the myelin sheath surrounding the axons, which is necessary for fast impulse conduction. Onset, progress, and consequences of the inflammatory demyelinating disease of the human peripheral nervous system, the Guillain-Barre-Syndrome (GBS), can be studied in its animal counterpart experimental autoimmune neuritis (EAN). EAN can be actively induced by immunization with the myelin proteins P2, PO, or peptides contained in them, or adoptively transferred by neuritogenic T-cells (AT-EAN).
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