Fig. 6

CSF IgG1 glycosylation correlates with intrathecal signs of inflammation within the MS group. IgG1 glycosylation in CSF, normalized to serum, is plotted against the CSF cell count (a) and intrathecal IgG fraction calculated by the Reiber formula (b) from MS patients (orange triangles). For comparison, also data from control donors (blue circles) are plotted. Correlation analysis was performed only within the MS group; ϱ and p values (Spearman’s method) are indicated. Trendlines represent LOWESS lines (Cleveland 1979) and indicate the strength of association (Spearman’s ϱ) by their opacity and thickness. Where appropriate (galactosylation and afucosylation vs. CSF cell count), an additional hyperbolic model was fitted as indicated. a CSF cell count. The strongest correlation was observed for afucosylated IgG1 vs. CSF cell count, which remained significant after correction for multiple testing. The correlation for galactosylation and bisecting GlcNAc was only present as a trend (significant only without adjustment for multiple testing). b Intrathecal IgG fraction. Likewise, the strongest correlation was observed for afucosylated IgG1 vs. IF_IgG, which remained significant after correction for multiple testing. Correlations for bisecting GlcNAc and galactosylation were present only as a trend. a, b The direction of the correlations paralleled the alteration in CSF from the MS group compared to controls (indicated in the lower left corner of each diagram): e.g., a lower fraction of CSF IgG1 was afucosylated in the MS group compared to controls, and this decrease was more pronounced in those patients with a higher-intrathecal IgG synthesis