Science Advances

Supplementary Materials

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  • Fig. S1. Liganding VSIG4 by complement C3b results from decreasing NLRP3 and proIL-1β expression in macrophages.
  • Fig. S2. The expression of NLRP3 and IL-1β in Vsig4−/− PEMs was not affected by VG11 mAbs.
  • Fig. S3. Vsig4 deficiency does not cause spontaneous NLRP3 inflammasome activation and IL-1β secretion.
  • Fig. S4. MS4A6D interacts with VSIG4 by using a yeast split-ubiquitin screen.
  • Fig. S5. Gating strategies of flow cytometry.
  • Fig. S6 Inhibition of NLRP3 activity or blocking IL-1β signaling controls the progress of EAE and colitis.
  • Fig. S7. Vsig4−/− mice are resistant to 2.5% DSS-induced colitis.
  • Fig. S8. Vsig4−/Il-1R1−/− mice deteriorated DSS-induced colonic damage.
  • Fig. S9. Model of VSIG4/MS4A6D signaling complex attenuates NLRP3 inflammasome activation.
  • Fig. S10. Creating Ms4a6d−/− mice by CRISPR/Cas9-mediated genome engineering.
  • Table S1. The PCR primers used in this study.

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