Guillain–Barré syndrome (GBS) represents a spectrum of acute immune-mediated neuropathies affecting the peripheral nervous system. It is clinically characterized by ascending muscle weakness, areflexia, sensory abnormalities, and, in severe cases, respiratory failure and autonomic instability. GBS remains the leading cause of acute flaccid paralysis worldwide, with an incidence of approximately 1–2 cases per 100,000 population annually.

Although the clinical presentation of GBS is well recognized, its underlying molecular mechanisms are complex and multifactorial. The disease is often preceded by infectious triggers, most notably Campylobacter jejuni, cytomegalovirus, Epstein–Barr virus, and Zika virus. These infections initiate aberrant immune responses through molecular mimicry, resulting in the generation of autoantibodies and immune cells that target peripheral nerve components.

Current therapeutic strategies—primarily intravenous immunoglobulin (IVIg) and plasma exchange—aim to broadly suppress or remove pathogenic immune factors. While effective in reducing disease severity and duration, these treatments do not specifically target the molecular signaling events driving nerve injury. Moreover, a significant proportion of patients experience incomplete recovery or long-term disability, highlighting the need for more precise therapeutic interventions.