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Acknowledgements
This study was supported by the National Institute of Neurological Disorders and Stroke (NIH/NINDS; Grants R01 NS42888, R01 NS54962, R21NS087467). We would like to thank Dr. Sally Ward (Texas A&M Health Science Center) for kindly providing us with Abdge (MST-HN) and Hulys10 antibodies.
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401_2017_1730_MOESM1_ESM.tif
Supplementary Fig. 1: Abdeg does not alter endoneurial innate immune responses, but decreases the amount of IgG in the endoneurium. (a) Immunofluorescence images showing decreased IgG deposition in Abdeg-treated nerve compared with control Ab (Hulys10)-treated nerve. Scale bar, 20 µm. (b) Quantification showing significant decrease of IgG level in Abdeg-treated nerves. n = 20. (c) Immunofluorescence images showing FcγRs (Fcγ common chain; Red) and macrophages (CD68; Green) in the injured sciatic nerves of animal treated with Hulys10 (Top) or Abdeg (Bottom). Scale bar, 20 µm. (d) Quantitative analysis of macrophage number in endoneurium and Fcγ common chain expression. n = 20. (e) Mean fluorescence intensity of activating FcγRs expression. n = 20 (TIFF 2597 kb)
401_2017_1730_MOESM2_ESM.tif
Supplementary Fig. 2: Schematic diagram showing the possible pathogenic mechanisms of anti-ganglioside Ab (AGA)-mediated nerve injury and how Abdeg treatment potentially interrupts ABG- FcγRs-macrophage axis in the endoneurium (TIFF 1982 kb)
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Zhang, G., Lin, J., Ghauri, S. et al. Modulation of IgG–FcRn interactions to overcome antibody-mediated inhibition of nerve regeneration. Acta Neuropathol 134, 321–324 (2017). https://doi.org/10.1007/s00401-017-1730-x
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DOI: https://doi.org/10.1007/s00401-017-1730-x