Cytokine production and the pathogenesis of experimental autoimmune neuritis and Guillain-Barre syndrome.

摘要

Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barre syndrome, GBS) and its animal model experimental autoimmune neuritis (EAN) are prototypes of T cell-mediated autoimmune diseases affecting the peripheral nervous system (PNS). Perivascular accumulation of macrophages and T lymphocytes in the PNS, and high levels systemically of PNS myelin antigen-reactive T cells are characteristic features of both diseases, thereby suggesting a pathogenic role for immunoregulatory cytokines. Here we summarise recent studies that have clearly documented that Th1/Th2/Th3 cytokines are differently upregulated during various clinical phases of EAN and GBS. The observations indicate that the role of cytokines in immune regulation and autoimmune disease is more complex than a simple Th1-Th2 dichotomy would suggest. New treatments may be searched for that counteract this complex cytokine imbalance. Treatments with antibodies that selectively target certain pro-inflammatory cytokines, as well as with immunomodulatory preparations that promote cytokines that beneficially influence the disease course should be in focus of future therapeutic trials.