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@castltrastondrs.medsky.network Oct 11, 2026, 5:13 AM

#GuillainBarrésyndrome (GBS) can be triggered by several viral and bacterial pathogens that induce peripheral nerve damage through immune-mediated mechanisms such as molecular mimicry

link.springer.com/article/10.1...

link.springer.com/chapter/10.1...

www.researchgate.net/publication/...

Representation of molecular mimicry, pathophysiological mechanism of GBS. The pathophysiology of GBS is evidenced by the mechanism of molecular mimicry, in which the virus shares epitopes common to neuron components, such as the myelin sheath and axonal lining. Thus, direct virus infection triggers the activation of the immune system and APC precursor cells, which differentiate into T and B lymphocytes. Also, the viral epitope is recognized by the B lymphocyte and the T lymphocyte releases isoleucine such as IL-6 and interleukin 4 (IL-4), in addition to cytokines such as TNF-α and interferon-gamma (IFN-γ) for macrophage activation, triggering local inflammation that can be exacerbated. Thus, there is the production of antibodies (ANTI-GM1) to attack the virus, however, by sharing epitopes, these antibodies also attack components of the neuron. The recruitment of more macrophages increases inflammation, as well as the performance of the microglia that release cytokines such as IFN-γ and interleukin 1 beta (IL-1β). Finally, the neuron is in hyperinflammation and operates with its reduced functionality or loses it definitively, being able to suffer cell death and causing irreversible damage to the patient with this syndrome

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