TY - JOUR
T1 - Ganglioside-specific IgG and IgA recruit leukocyte effector functions in Guillain-Barré syndrome
AU - van Sorge, Nina M.
AU - Yuki, Nobuhiro
AU - Koga, Michiaki
AU - Susuki, Keiichiro
AU - Jansen, Marc D.
AU - van Kooten, Cees
AU - Wokke, John H. J.
AU - van de Winkel, Jan G. J.
AU - van der Pol, W. Ludo
AU - van den Berg, Leonard H.
PY - 2007/1
Y1 - 2007/1
N2 - The capacity of ganglioside-specific autoantibodies to recruit leukocyte effector functions was studied. Serum samples from 87 patients with Guillain-Barré (GBS) or Miller Fisher syndrome (MFS), containing GM1-, GQ1b-, or GD1b-specific IgG or IgA, were tested for leukocyte activating capacity. Ganglioside-specific IgG antibodies generally induced leukocyte activation, irrespective of specificity. The magnitude of leukocyte degranulation correlated with GM1- and GQ1b-specific IgG titers, but not with disease severity. Finally, GM1-specific IgA activated leukocytes through the IgA receptor, FcαRI (CD89). Therefore, both ganglioside-specific IgG and IgA can recruit leukocyte effector functions, which may be relevant in the pathogenesis of GBS and MFS. © 2006 Elsevier B.V. All rights reserved.
AB - The capacity of ganglioside-specific autoantibodies to recruit leukocyte effector functions was studied. Serum samples from 87 patients with Guillain-Barré (GBS) or Miller Fisher syndrome (MFS), containing GM1-, GQ1b-, or GD1b-specific IgG or IgA, were tested for leukocyte activating capacity. Ganglioside-specific IgG antibodies generally induced leukocyte activation, irrespective of specificity. The magnitude of leukocyte degranulation correlated with GM1- and GQ1b-specific IgG titers, but not with disease severity. Finally, GM1-specific IgA activated leukocytes through the IgA receptor, FcαRI (CD89). Therefore, both ganglioside-specific IgG and IgA can recruit leukocyte effector functions, which may be relevant in the pathogenesis of GBS and MFS. © 2006 Elsevier B.V. All rights reserved.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=33845923931&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/17156858
U2 - https://doi.org/10.1016/j.jneuroim.2006.10.015
DO - https://doi.org/10.1016/j.jneuroim.2006.10.015
M3 - Article
C2 - 17156858
SN - 0165-5728
VL - 182
SP - 177
EP - 184
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -