Supplementary Materials

Supplementary Material for:

The Circulating Proteinase Inhibitor α-1 Antitrypsin Regulates Neutrophil Degranulation and Autoimmunity

David A. Bergin, Emer P. Reeves,* Killian Hurley, Rebecca Wolfe, Ramia Jameel, Sean Fitzgerald, Noel G. McElvaney

*Corresponding author. E-mail: emerreeves@rcsi.ie

Published 1 January 2014, Sci. Transl. Med. 6, 217ra1 (2014)
DOI: 10.1126/scitranslmed.3007116

This PDF file includes:

  • Fig. S1. Equal tertiary and secondary granule protein expression in MM and ZZAATD neutrophils.
  • Fig. S2. TNF-α exposure for 20 min does not induce apoptosis in MM or ZZAATD neutrophils.
  • Fig. S3. Physiological and acute-phase levels of AAT modulate TNF-α–induced degranulation.
  • Fig. S4. IgM autoantibodies against granule proteins in ZZ-AATD.
  • Fig. S5. Augmentation therapy does not affect soluble plasma levels of TNFR2.
  • Fig. S6. Loading controls for Western blots analyzing healthy control (MM) and ZZ-AATD neutrophil degranulation.
  • Fig. S7. Loading controls for Western blots analyzing the effect of AAT compared to antithrombin III on neutrophil degranulation.
  • Fig. S8. Isotype controls for flow cytometry analysis of MM and ZZ-AATD neutrophils for TNF-α, lactoferrin, AAT, and CD66b.
  • Fig. S9. Isotype control for flow cytometry analysis of the ability of AAT to modulate neutrophil membrane TNF-α interaction.

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