Acute Inflammatory Demyelinating Polyradiculoneuropathy AIDP

T cell activation in BAN is accompanied by expression of inflammatory cytokines such as IBN-y, TNF-a, TNF-(3, IL-6 and IL-12 (Zhu et al., 1994, 1997). In sera of GBS, inflammatory cytokines detected include IBN-y, TNF-a andIL-2, which are increased in patients and partially correlate with disease 

Because macrophages represent the major cell population in infildrates of affected nerves, they are considered to be key mediators of injury to myelin, Schwann cells, and axons. This hypothesis is reinforced by experimental studies, where depletion of macrophages prevents the development of BAN. Although endoneurial macrophages are present in 

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Figure 20.1. Hypothetical scheme of the immune response in acute inflammatory demyelinating polyradiculoneuropathy (AIDP) Inflammatory cells migrate from the systemic immune compartment through the damaged blood-nerve barrier into the endoneurium. Inflammatory infiltrates, which contain T-lymphocytes and macrophages cause marked segmental demyelination and secondary axonal degeneration (B B-cell T T-cell M4> Macrophage).

AID AIDP AIDS AIF AIRE AIS AES AMAN AMN AMPA AMSAN activation-induced (cytidine) deaminase acute inflammatory demyelinating polyradiculoneuropathy acquired immunodeficiency syndrome apoptosis inducing factor autoimmune regulator anterior chamber associated immune deviation (ACAID)-inducing signal amyotrophic lateral sclerosis acute motor axonal neuropathy adrenomyeloneuropathy a-amino-3 -hydroxy-5-methylisoxazole- 4-propionic acid acute motor-sensory axonal neuropathy... 

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