Supplementary Materials

Supplementary Materials for:

The TNF Family Member 4-1BBL Sustains Inflammation by Interacting with TLR Signaling Components During Late-Phase Activation

Jianhui Ma, Bo-Ram Bang, Jiawei Lu, So-Young Eun, Motoyuki Otsuka, Michael Croft, Peter Tobias, Jiahuai Han, Osamu Takeuchi, Shizuo Akira, Michael Karin, Hideo Yagita, Young Jun Kang*

*Corresponding author. E-mail: ykang@scripps.edu

This PDF file includes:

  • Fig. S1. Cross-linking of 4-1BBL stimulates TNF-α production by macrophages.
  • Fig. S2. Involvement of TRAF6 in the 4-1BBL–mediated production of TNF-α.
  • Fig. S3. The 4-1BBL–mediated inflammatory response does not require NF-κB signaling.
  • Fig. S4. 4-1BBL–induced TNF-α production is mediated by the activation of protein kinase signaling pathways.
  • Fig. S5. TIRAP, but not Tollip, interacts with 4-1BBL to stimulate downstream signaling.
  • Fig. S6. Specific inhibition of TIRAP activity by the TIRAP inhibitory peptide.
  • Fig. S7. Inhibition of sustained TNF-α production by an anti–4-1BBL antibody.
  • Fig. S8. Formation of a 4-1BBL–TIRAP–TRAF6–TAK1–TAB1 complex.
  • Fig. S9. 4-1BBL physically associates with IRAK2.
  • Fig. S10. IRAK4 physically interacts with IRAK2 but not 4-1BBL.
  • Fig. S11. Amelioration of LPS-induced septic shock by inhibition of MyD88 activity.

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Citation: J. Ma, B.-R. Bang, J. Lu, S.-Y. Eun, M. Otsuka, M. Croft, P. Tobias, J. Han, O. Takeuchi, S. Akira, M. Karin, H. Yagita, Y. J. Kang, The TNF Family Member 4-1BBL Sustains Inflammation by Interacting with TLR Signaling Components During Late-Phase Activation. Sci. Signal. 6, ra87 (2013).

© 2013 American Association for the Advancement of Science