A way out of the maze

In the last decade, experimental and clinical studies have laid a solid foundation under the molecular mimicry hypothesis to explain the pathogenesis of the Guillain-Barré syndrome (GBS). Bacterial or viral infections and genetic host factors are important. In brief, in the weeks following infection with known and unknown micro-organisms, previously healthy persons develop a devastating acute inflammatory disease of the peripheral nervous system. The immune system of the patient is apparently deceived by bacterial ganglioside-like epitopes that mimic peripheral nerve components, thereby triggering a cascade of inflammatory responses against peripheral nerves. Cross-reactive anti-ganglioside antibodies may be directed against myelin, Schwann cell components, and axonal membranes.^1,2 Mechanisms by which damage is induced include activation of inflammatory cells by interaction of antibodies with Fcγ receptors (FcγRs) on macrophages and γ/δ T cells. Efficient FcγR-IgG interactions increase efficacy of leukocyte effector functions such as phagocytosis, cellular cytotoxicity, and cytokine production. FcγRIII genotypes are host factors that could modify severity of GBS.³ Also, an association has been found between polymorphisms in genes that are involved in immune homeostasis and the presence of …