MECHANISMS OF SCHWANN-CELL DAMAGE IN INFLAMMATORY NEUROPATHY

Inflammatory demyelination of nerve in Guillain-Barre syndrome is trig gered in most patients by prior infection with one of a series of orga nisms, including Campylobacter jejuni. The resulting inflammatory casc ade, involving T cells, macrophages, complement, and cytokines, disrup ts physiologic function of the peripheral nerve in part by targeting S chwann cells, the multipotential glial cells that synthesize multilame llar, compacted myelin and secrete growth factors. In vitro evidence s uggests that the Schwann cell may itself be able to modulate the casca de by serving as an antigen-presenting cell and by producing cytokines and other acute-phase reactants.