Additional Supporting Information may be found in the online version of this article.

HEP_23795_sm_SuppFig1.tif4681KSupporting Information Figure 1. No alterations of oxidant stress and CYP2E1 expression between WT and CX3CR1-deficient mice after CCl4 treatment. (A) Immunofluorescence for 4-hydroxy-nonenal (4-HNE)(original magnification: x200) and (B) Western blot for CYP2E1 in the livers from WT and CX3CR1-deficient mice after 12 injections of vehicle or CCl4 are shown.
HEP_23795_sm_SuppFig2.tif3224KSupporting Information Figure 2. AKT and ERK are required for CX3CL1-induced anti-inflammatory properties. WT Kupffer cells were pretreated with LY294002 (AKT inhibitor, 2 μM) or U0125 (ERK inhibitor, 20 μM) for 30 min, followed by treating with CX3CL1 (100 ng/ml) for additional 6 h. mRNA expression of IL-10 and arginase-1 was measured by qPCR. *p<;0.05, N.S. not significant.
HEP_23795_sm_SuppFig3.tif3299KSupporting Information Figure 3. CX3CL1 treatment inhibits LPS-induced cytokine production in Kupffer cells. WT Kupffer cells were treated with LPS (10 ng/ml) for 6 h, in the presence or absence of CX3CL1 (100 ng/ml). mRNA expression of TNF-α and TGF-β was measured by qPCR. *p<0.05,
HEP_23795_sm_SuppFig4.tif4885KSupporting Information Figure 4. CX3CR1 expression in hepatic NK cells and T cells. Liver mononuclear cells isolated from vehicle or CCl4-treated CX3CR1+/GFP mice, were stained with anti-NK1.1 and CD3 antibody followed by FACS analysis for detecting the expression of NK1.1, CD3 and GFP as endogenous CX3CR1 expression. Representative FACS analysis is shown (n=3).
HEP_23795_sm_SuppTable1.doc21KSupporting Information Table 1.

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