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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-Barre 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 …