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Indoxyl sulfate (IS)-mediated immune dysfunction provokes endothelial damage in patients with end-stage renal disease (ESRD)

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Table 1.  Clinical characteristics of ESRD patients and healthy control subjects. ESRD, end-stage renal disease;  CAD, coronary artery disease; DM, diabetes mellitus; BMI, body mass index; BUN, blood urea nitrogen; SBP,  systolic blood pressure; DBP, diast
Figure 3.  IS-induced TNF-α expression is regulated through AhR activation in human monocytes
Figure 4. TNF-α markedly upregulates CX3CL1 production by HUVECs. (A) HUVECs were stimulated  with TNF-α (5 ng/ml) up to 8 hours and CX3CL1 mRNA expression was analyzed by real-time RT-PCR at  the indicated time-points
Figure 5. CD4 + CD28 −  T cells expressing CX3CR1, a receptor for CX3CL1, are expanded under the TNF-α  rich environment in ESRD patients
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