Molecular Mimicry in Guillain-Barre Syndrome
- Molecular Mimicry is the condition where immune system gets confused between “self” and “non-self” antigens due to molecular similarities between an environmental agent (bacteria and virus most commonly) and the host. Molecular mimicry can explain pathogenesis of few autoimmune diseases and this post is about Guillain-Barre Syndrome (GBS).
- Guillain-Barre Syndrome is characterized by an immune-mediated attack on peripheral nerve, more commonly in the myelin sheath or Schwann cells of sensory and motor nerves.
- Infection with few pathogens leads to the production of antibodies to a carbohydrate-containing surface antigen that cross-reacts with the myelin sheath and the axons of nerve cells, resulting in demyelination and axonal degeneration.
- Antibody and/or cell-mediated immune responses are involved in degeneration of the nerve and interruption of neurotransmission which is responsible for muscle weakness.
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GBS the Immune-mediated polyneuropathy has many variant forms
- Acute inflammatory demyelinating polyneuropathy (AIDP) most common form
- Chronic inflammatory demyelinating polyneuropathy (CIDP)
- Miller Fisher syndrome
- Acute motor axonal neuropathy (AMAN)
- Acute motor sensory axonal neuropathy (AMSAN)
- Approximately 70-80% of cases of GBS occur few weeks after an acute infection, usually respiratory or gastrointestinal.
Pathogens associated with GBS
- Campylobacter jejuni is most common associated pathogen- An important source of infection is contaminated food. Poultry products are often colonized with C. jejuni and are major food-borne vehicle for campylobacteriosis.
- Mycoplasma pneumoniae
- HIV
- CMV
- Ebstein-Barr virus (EBV)
- Zika virus
Summary
Similar antigens---Confusion between self and non-self---attack on myelin sheath ----impaired neurotransmission----muscle weakness----GBS
- Further reading https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1698092/
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