Supplementary information
From the following article
Sushil Kumar Pathak, Sanchita Basu, Kunal Kumar Basu, Anirban Banerjee, Shresh Pathak, Asima Bhattacharyya, Tsuneyasu Kaisho, Manikuntala Kundu & Joyoti Basu
Nature Immunology 8, 610 - 618 (2007) Published online: 7 May 2007
doi:10.1038/ni1468
Supplementary Fig. 1
ESAT-6-dependent effects on RAW264.7 macrophages are not due to IL-10 induction and ESAT-6 does not modulate TLR ligand-dependent TLR-MyD88 interactions.
Supplementary Fig. 2
ESAT-6 inhibits the interaction of MyD88 with IRAK-4.
Supplementary Fig. 3
ESAT-6 does not induce MyD88s or IRAK-M, nor does it alter expression of TLRs and negative regulators of TLR signaling.
Supplementary Fig. 4
ESAT-6-mediated attenuation of IL-12 p40 release does not require TLR1, TLR6 or CD14 and ESAT-6 attenuates TLR ligand-induced IRAK-4 kinase activity in a PI-3K/Akt-dependent manner.
Supplementary Fig. 5
ESAT-6 interacts directely with the extracellular domain (ECD) of TLR2.
Supplementary Fig. 6
ESAT-6 inhibits TLR ligand-induced activation of IKK
kinase activity, LPS-driven activation of p38 MAPK and nuclear translocation of IRF-3 in RAW cells.
Supplementary Fig. 7
The C terminus of ESAT-6 inhibits TLR ligand induced nuclear translocation of IRFs 5, 1 and 3, binds to the surface of RAW cells and inhibits TLR ligand-induced IL12p40 production in bone marrow derived macrophages (BMDMs).
Supplementary Table 1
Sequences of overlapping peptides of ESAT-6.
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