Immunopathogenesis and treatment of the guillain‐barré syndrome—part I

Abstract

The etiology of the Guillain-Barré syndrome (GBS) still remains elusive. Recent years have witnessed important advances in the delineation of the mechanisms that may operate to produce nerve damage. Evidence gathered from cell biology, immunology, and immunopathology studies in patients with GBS and animals with experimental autoimmune neuritis (EAN) indicate that GBS results from aberrant immune responses against components of peripheral nerve. Autoreactive T lymphocytes specific for the myelin antigens P0 and P2 and circulating antibodies to these antigens and various glycoproteins and glycolipids have been identified but their pathogenic role remains unclear. The multiplicity of these factors and the involvement of several antigen nonspecific proinflammatory mechanisms suggest that a complex interaction of immune pathways results in nerve damage. Data on disturbed humoral immunity with particular emphasis on glycolipid antibodies and on activation of autoreactive T lymphocytes and macrophages will be reviewed. Possible mechanisms underlying initiation of peripheral nerve-directed immune responses will be discussed with particular emphasis on the recently highlighted association with Campylobacter jejuni infection.

The fatty acid transport function of fatty acid-binding proteins

“…Despite the decrease in LCFA oxidation, however, the LFABP null mouse does not develop hepatosteatosis following either a high fat diet or an overnight fast, as found for wild type controls, indicating protection against development of the metabolic syndrome, although others report an exacerbation of obesity (27). Recently, it was shown that LFABP null mice were highly susceptible to the development of cholesterol gallstones, with the effect likely secondary to increased liver cholesterol levels and increased enterohepatic bile acid pool size (28).…”

Th1-like responses to peptides from peripheral nerve myelin proteins in patients with polyneuropathy associated with monoclonal gammopathy

“…Thus, other mechanisms, besides the M-protein acting as antibodies, may be operating. In another demyelinating polyneuropathy, the Guillain-Barré syndrome (GBS), T cell-mediated mechanisms are proposed ( [11,12]; Dahle et al, data to be published). There are some reports suggesting that T cells also may be involved in the pathogenesis of polyneuropathy associated with monoclonal gammopathy.…”

Paraneoplastic Neurologic Syndrome: Three Case Reports

“…It is considered that both humoral and cellular immunity play a role in the development of the disease (21,22). GBS mostly develops secondary to the respiratory and gastrointestinal system infections or vaccination.…”