IMMUNOPATHOGENESIS AND TREATMENT OF THE GUILLAIN-BARRE-SYNDROME .1.

The etiology of the Guillain-Barre syndrome (GBS) still remains elusiv e. Recent years have witnessed important advances in the delineation o f the mechanisms that may operate to produce nerve damage, Evidence ga thered from cell biology, immunology, and immunopathology studies in p atients with GBS and animals with experimental autoimmune neuritis (EA N) indicate that GBS results from aberrant immune responses against co mponents of peripheral nerve, Autoreactive T lymphocytes specific for the myelin antigens PO and P2 and circulating antibodies to these anti gens and various glycoproteins and glycolipids have been identified bu t their pathogenic role remains unclear, The multiplicity of these fac tors and the involvement of several antigen nonspecific proinflammator y mechanisms suggest that a complex interaction of immune pathways res ults in nerve damage, Data on disturbed humoral immunity with particul ar emphasis on glycolipid antibodies and on activation of autoreactive T lymphocytes and macrophages will be reviewed. Possible mechanisms u nderlying initiation of peripheral nerve-directed immune responses wil l be discussed with particular emphasis on the recently highlighted as sociation with Campylobacter jejuni infection. (C) 1995 John Wiley and Sons, Inc.