Fig. S1. Expression of cell surface activation markers on murine B cells following in-vivo poly I:C administration. C57BL/6 (B6) mice were injected intraperitoneally (i.p.) with lipopolysaccharide (LPS). On days 0 and 1 post-injection, the mice were examined for the expression of the indicated surface molecules on spleen versus hepatic B cells; n = 4 mice per group. On day 1, both liver and splenic B cells up-regulated expression of CD39, CD40, CD80 and CD86; *P < 0·05. No significant difference was observed between the liver and spleen. Data are representative of two independent experiments.

Fig. S2. Close proximity of B cells (CD19+) and dendritic cells (DCs) (CD11c+) in liver parenchyma. Cryostat sections (5 μm) of liver tissue samples from fms-like tyrosine kinase 3 ligand (Flt3L)-treated B6 mice were stained for B cells (CD19; green), DCs (CD11c; red) and nuclei (DRAQ5; blue). Fluorescent images were captured with an Olympus Fluoview 1000 confocal microscope (software version 1·7a).

Fig. S3. Splenic, but not hepatic, B cells inhibit the activation of liver myeloid dendritic cells (mDCs) in response to lipopolysaccharide (LPS) in vitro. B cell-depleted liver non-parenchymal cells (NPC) isolated from fms-like tyrosine kinase 3 ligand (Flt3L)-treated B6 mice were cultured with or without LPS in the presence or absence of hepatic or splenic B cells for 48 h. Activation of mDCs was analysed by expression of CD80, CD86 and programmed cell death 1 ligand 1 (PD-L1) on CD19B220CD3CD11c+ mDCs. Liver mDCs in the presence of B cells were compared with those in the absence of B cells; **P < 0·01.

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