Supplementary Materials

Supplementary Material for:

An increase in LRRK2 suppresses autophagy and enhances Dectin-1–induced immunity in a mouse model of colitis

Tetsuya Takagawa, Atsushi Kitani, Ivan Fuss, Beth Levine, Steven R. Brant, Inga Peter, Masaki Tajima, Shiro Nakamura, Warren Strober*

*Corresponding author. Email: wstrober{at}niaid.nih.gov

Published 6 June 2018, Sci. Transl. Med. 10, eaan8162 (2018)
DOI: 10.1126/scitranslmed.aan8162

This PDF file includes:

  • Materials and Methods
  • Fig. S1. LRRK2 protein expression in representative LCLs determined by Western blots.
  • Fig. S2. Additional information about DSS-induced colitis in Lrrk2 Tg and Lrrk2 KO mice.
  • Fig. S3. BMDCs from Lrrk2 Tg mice exhibit higher production of IL-23 than BMDCs from control mice in response to Dectin-1 agonists.
  • Fig. S4. BMDCs from Lrrk2 KO mice do not produce increased TNF-α compared to BMDCs from Lrrk2 WT mice.
  • Fig. S5. LRRK2 positively regulates NFAT activity.
  • Fig. S6. Increased autophagy in BMDCs from Lrrk2 KO mice.
  • Fig. S7. Inhibitory effects of 12 LRRK2 inhibitors.
  • Fig. S8. IL-2 production by Lrrk2 Tg mouse and control BMDCs was suppressed by LRRK2 inhibitors.
  • Fig. S9. LRRK2 inhibitors suppressed a broad range of cytokines produced by mouse BMDCs.
  • Fig. S10. BMDCs from Lrrk2 Tg mice exhibited increased autophagy when cultured with a LRRK2 inhibitor (LRRK2-IN-1).
  • Fig. S11.The LRRK2 Inhibitor LRRK2-IN-1 ameliorated DSS-induced colitis in C57BL/6J mice.
  • Fig. S12. Severity of DSS-induced colitis in control mice on a C57BL/6J background varied with housing conditions.
  • Fig. S13. Summary diagram.
  • Table S1. Characteristics of CD patients.
  • Table S2. Eighteen LCLs used in this study.
  • Reference (54)

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Other Supplementary Material for this manuscript includes the following:

  • Table S3 (Microsoft Excel format). Individual level data.