Guillain-Barre syndrome (CBS) is an immune-mediated acute inflammatory disorder in the peripheral nervous system (PNS) of humans characterized by inflammatory infiltration and damage to myelin and axon. Experimental autoimmune neuritis (EAN) is a useful animal model for CBS. Although CBS and EAN have been widely studied, the pathophysiological basis of GBS/EAN remains largely unknown. Immunocompetent cells together with cytokines produced by various cells contribute to the inflammatory process of EAN by acting as mediators or effectors. Both CBS and EAN have hitherto been attributed to T helper (Th)1 cells-mediated disorders, however, some changes in CBS and EAN could not be explained by the pathogenic role of Th1 cells and a disturbance of the Th1/Th2 balance, which has previously been considered to be important for the homeostatic maintenance of the immune responses and to explain the adaptive immunity and autoimmune diseases. The Th1/Th2 paradigm in autoimmune diseases has been greatly challenged in recent years, with the identification of a particular T cell subset Th17 cells. Studies on the associations between Th17 cells/cytokines and GBS/EAN are reviewed. But some of them occasionally yield conflicting results, indicating an intricate network of cytokines in immune response. (C) 2013 Elsevier Ltd. All rights reserved.
[1]Jilin Univ, Hosp 1, Dept Neurol, Changchun, Peoples R China.
[2]Karolinska Inst, Dept Neurobiol Care Sci & Soc, Stockholm, Sweden.
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