Pathophysiology of Guillain-Barré Syndrome

       The mechanism of how the infection, vaccination, trauma, or other factors that precipitate the occurrence of acute demyelination in GBS is still not known with certainty. Many experts conclude that the nerve damage that occurs in this syndrome is through immunologic mechanisms. Evidence that the immunopathogenesis which is the mechanism that causes peripheral nerve injury in this syndrome are:

1. Acquired antibodies or a cellular immune response (cell mediated immunity) against infectious agents in the peripheral nerves.
2. The presence of auto antibodies to the peripheral nervous system.
3. Obtainment hoarding antigen antibody complexes from the circulation of the blood vessels of peripheral nerves that causes  peripheral nerve demyelinating processes.

       The process of peripheral nerve demyelination in GBS is influenced by the response of cellular immunity and humoral immunity triggered by previous events. In GBS, ganglioside is a target of the antibody. Association of antibodies in the body's immune system activates a breakdown of myelin. The reason why the normal component of myelin fibers is a target of the immune system are not known, but infection by viruses and bacteria is suspected as the cause of the antibody response of the immune system. It is obtained from the lipopolysaccharide layer of ganglioside similar to the human body. Campylobacter jejuni, a bacterial pathogen that causes diarrhea, it contains a membrane protein which is a clone of the ganglioside GM1. In the case of infection by Campylobacter jejuni, damage occurred mainly in axon degeneration. Changes in the axons contributing to cross-reacting antibodies to ganglioside GM1 forms to respond to the same epitope. Based on the signal humoral immunity infection menginisisasi the T-cell response in the presence of lymphocytic infiltration into the spinal and peripheral nerves. Formed macrophages in the area of damage and cause demyelination processes and delivery barriers nerve impulses.

Role of cellular immunity
       In the cellular immune system, T lymphocytes play an important role in addition to the role of macrophages. Lymphocyte precursor cells derived from bone marrow (bone marrow) cells undergo maturation steam before it is released into the circulation and lymphoid tissues.

      Before this cellular immune response occurs in peripheral nerve antigen must be introduced in T lymphocytes (CD4) by macrophages. Macrophages that had swallowed (phagocytosis) antigen / stimulated by viruses, allergens or other ingredients ImmunoGen will process these antigens by the antigen presenters (antigen presenting cell = APC). Then the antigen will be introduced in T lymphocytes (CD4). After that the T lymphocytes become activated because the activation marker and release substances interlekuin (IL2), interferon gamma and TNF alpha.

       Solubility E selectin and adhesion molecules (ICAM) generated by the activation of endothelial cells will play a role in opening the blood nerve cells to activate T lymphocytes and macrophages decision. Macrophages will secrete proteases that can damage myelin protein disampin produce TNF and complement.


•    Guillain-Barre Syndrome•    Etiology of Guillain–Barré Syndrome•    Clinical Manifestations of Guillain-Barré Syndrome•    Medical Treatment and Therapy of Guillain–Barré syndrome•    How to Diagnose Guillain–Barré syndrome
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