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. 2018 Nov 27;6(1):129–143. doi: 10.1002/acn3.687

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© 2018 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Patients with high plasmablast numbers after IVIg treatment have high GM1 IgG titers at onset. Pre‐ and posttreatment sera from GBS patients positive for GM1 IgG antibodies (n = 12) were titrated by ELISA. Data is shown stratified according to low or high plasmablast count assessed 1 week after IVIg treatment (A). A titer of <100 is considered negative. Two‐way ANOVA followed by Bonferroni correction (***P < 0.001). Subclass analysis of anti‐GM1 antibodies (B–E) demonstrated that the majority of patients do not produce anti‐GM1 antibodies of the IgG2 subclass; only one patient is positive for anti‐GM1 IgG2 1 week after treatment (C). The dotted line indicated the cutoff value (ΔOD = 0.2).