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. 2012 Dec 4;79(23):2241–2248. doi: 10.1212/WNL.0b013e31827689ad

Figure 3. Features of antibodies to neurofascin (NF) in a patient with chronic inflammatory demyelinating polyneuropathy (CIDP).

Figure 3

Reactivity to NF155 was seen by flow cytometry (A–C) up to a dilution of 1:10,000 (B). (A) Reactivity to NF155 (blue line) was compared with reactivity to NF186 (orange line) and to control cells (black, filled). (B) The mean fluorescence intensity (MFI) ratio is plotted for level of reactivity above background. (C) The NF155 reactivity was mediated by immunoglobulin (Ig)G4 with minor contribution from IgG1. Reactivity to NF155 was also seen by ELISA (D–F) up to a dilution of 1:10,000 (E) by IgG4 and weakly by IgG1, IgG3, IgM, and IgA (F). Serum staining (G, left) colocalizes with Caspr staining (G, middle) on longitudinal rat spinal cord sections. The scale bar represents 10 μm. (H) NF186 differs from NF155 by substitution of Fn3-Fn4 with Fn4-Mucin-Fn5 (Ig = immunoglobulin-like domain; Fn = fibronectin type III domain). (I) A scheme of super green fluorescent protein (sGFP) fusion truncated NF variants is shown beside the corresponding serum reactivity by flow cytometry. Reactivities to truncated NF variants and to negative control cells are shown as sGFP intensity vs serum reactivity. The fragment recognized by both NF155-reactive serum samples is boxed.