Antibody of patients with Guillain-Barré syndrome mediates complement-dependent cytolysis of rat Schwann cells: Susceptibility to cytolysis reflects Schwann cell phenotype

1994 ◽  
Vol 49 (1-2) ◽  
pp. 145-152 ◽  
Author(s):  
Suneeti Sawant-Mane ◽  
Alden Estep ◽  
Carol Lee Koski
1996 ◽  
Vol 92 (4) ◽  
pp. 386-394 ◽  
Author(s):  
M. T. Berciano ◽  
E. Calle ◽  
M. A. Andres ◽  
J. Berciano ◽  
M. Lafarga

2020 ◽  
Vol 25 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Madeleine E. Cunningham ◽  
Gavin R. Meehan ◽  
Sophie Robinson ◽  
Denggao Yao ◽  
Rhona McGonigal ◽  
...  

Neurology ◽  
1984 ◽  
Vol 34 (9) ◽  
pp. 1240-1240 ◽  
Author(s):  
R. P. Lisak ◽  
D. Kuchmy ◽  
P. J. Armati-Gulson ◽  
M. J. Brown ◽  
A. J. Sumner

2021 ◽  
Vol 12 ◽  
Author(s):  
Kathleen M. Hagen ◽  
Shalina S. Ousman

Guillain-Barré syndrome (GBS) is a paralyzing autoimmune condition affecting the peripheral nervous system (PNS). Within GBS there are several variants affecting different aspects of the peripheral nerve. In general, there appears to be a role for T cells, macrophages, B cells, and complement in initiating and perpetuating attacks on gangliosides of Schwann cells and axons. Of note, GBS has an increased prevalence and severity with increasing age. In addition, there are alterations in immune cell functioning that may play a role in differences in GBS with age alongside general age-related declines in reparative processes (e.g., delayed de-differentiation of Schwann cells and decline in phagocytic ability of macrophages). The present review will explore the immune response in GBS as well as in animal models of several variants of the disorder. In addition, the potential involvement of an aging immune system in contributing to the increased prevalence and severity of GBS with age will be theorized.


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