Science Immunology

Supplementary Materials

Supplementary Material for:

ZBP1/DAI is an innate sensor of influenza virus triggering the NLRP3 inflammasome and programmed cell death pathways

Teneema Kuriakose, Si Ming Man, R. K. Subbarao Malireddi, Rajendra Karki, Sannula Kesavardhana, David E. Place, Geoffrey Neale, Peter Vogel, Thirumala-Devi Kanneganti*

*Corresponding author. Email: thirumala-devi.kanneganti{at}

Published 12 August 2016, Sci. Immunol. 1, aag2045 (2016)
DOI: 10.1126/sciimmunol.aag2045

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Cell death induced by IAV infection in BMDMs occurs independently of MyD88, MAVS, TRIF, STING, and TRADD but is dependent on the transcription factors STAT1 and IRF9.
  • Fig. S2. ZBP1 induced via IFN signaling regulates cell death in IAV-infected cells independently of virus load and IFN-β production.
  • Fig. S3. ZBP1 is dispensable for activation of canonical and noncanonical NLRP3, NLRC4, and AIM2 inflammasomes.
  • Fig. S4. IAV-induced cell death is not prevented by the absence of NLRP3, caspase-1, or gasdermin D.
  • Fig. S5. ZBP1 drives activation of complementary cell death pathways during IAV infection.
  • Fig. S6. ZBP1 is dispensable for proinflammatory cytokine production in response to other RNA viruses.
  • Fig. S7. ZBP1 is dispensable for cell death in response to transfected RNA and dsDNA ligands.
  • Table S1. Real-time quantitative PCR primer sequences.
  • Unmodified Western blots
  • Staining controls for confocal microscopy
  • Source data from in vivo infections (survival study and lung viral titers)

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Other Supplementary Material for this manuscript includes the following:

  • Source data from microarray analysis (Excel)
  • Source data from histopathological analysis (Excel)

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