![]() ![]() Humoral responses are initiated through activation of B cells by Th2 lymphocytes or by the epitopes of the virus cross-linking the B cell receptors. Macrophages initiate damage to PNS by producing and secreting matrix metalloproteinases (MMPs) and nitric oxide. Once inside the PNS, the Th1 phenotype of differentiated Th cell recruits and activates macrophages. Each phenotype has its specific cytokine signature and function. Stimulation of APCs results in T cell activation and differentiation into either a Th1 (T helper cell type 1) or Th2 phenotype. Epitopes displayed by the virus interact with pattern recognition receptors (PRRs) on APCs, especially DCs. Antigen-presenting cells (APCs) including dendritic cells (DCs), macrophages, and B lymphocytes are in the frontline dealing with the influenza infections. As previously mentioned, GBS begins with infectious agents such as influenza virus. The blood–nerve barrier is particularly leaky within the dorsal root ganglia and is altogether absent at nerve terminals, making these areas especially vulnerable to immune-mediated attacks. The blood–nerve barrier is not as tight as the blood–brain barrier, so that small amounts of circulating proteins and immunoglobulin G (IgG) can leak into PNS making it vulnerable to the immune attacks. ![]() IMMUNOPATHOLOGY OF GUILLAIN–BARRÉ SYNDROMEĪccess to the PNS by the immune system requires crossing of the blood–nerve barrier. Vaccination to influenza has been implicated in GBS, although the evidence for this link is controversial. Infection by Campylobacter jejuni is identified as the most common inciting event although other agents such as herpes simplex virus (HSV), cytomegalovirus (CMV), Epstein–Barr virus (EBV), Zika virus (ZIKV), Mycoplasma pneumoniae, Haemophilus influenza, and influenza have been reported. Severe autoimmune responses resulted from infections by external infectious agents are considered as major initiating factors of the syndrome. The estimated risk of developing GBS in the world is one to two cases per 100,000 people per year. The incidence of GBS increases with age, and people older than 50 years are at greatest risk for developing GBS. The mortality rate of the disease is approximately 8% in developing world, but much lower in developed countries. Although most people have an uneventful recovery, up to one-third of the cases are left with severe neurological deficits. The treatment includes administration of intravenous immunoglobulins or plasmapheresis, and supportive therapies. Diagnosis of this syndrome is based on the clinical signs and symptoms and through rule out of other differential diagnoses as shown in Table 1. The disease can be self-limiting, with muscle strength reaching a lowest point in few days, followed by a partial or full recovery over weeks to months. In some cases, GBS can affect the heart rate and changes the blood pressure by disrupting the autonomic nervous system. GBS may lead to respiratory failure requiring mechanical ventilation over 15% of cases. The initial symptoms of GBS include muscle weakness that starts from distal limbs which subsequently progresses to proximal limbs. This immune-mediated demyelinating neuropathy can rapidly evolve over a period of few days or more and can lead to paralysis or even death. GBS is an autoimmune disorder affecting the Schwann cells of the PNS. Since the eradication of polio, GBS has become the most common cause of acute flaccid paralysis. GUILLAIN–BARRÉ SYNDROME: SYMPTOMS AND CAUSES ![]()
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