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. Author manuscript; available in PMC: 2009 Nov 1.
Published in final edited form as: Hepatology. 2008 Nov;48(5):1440–1450. doi: 10.1002/hep.22500

Figure 3.

Figure 3

Figure 3

Association between chemokine expression and fibrosis and hepatitis C virus (HCV) genotype. Box and whisker plots illustrate differences in intrahepatic chemokine mRNA levels in patients according to differences in fibrosis stage for a) CXCL10 (interferon γ–inducible protein-10: IP-10), b) CXCL9 (monokine induced by interferon γ: Mig), and c) CXCL11 (interferon inducible T-cell alpha chemoattractant: I-TAC). Patients were grouped according to the fibrosis stage as none (stage = 0), minimal/mild (stage = 1), mild/moderate (stage = 2) and moderate/advanced (stage >2). CXCL10 levels are significantly (p = 0.05) elevated in those with stage = 0 compared to those with stage > 2. CXCL9 and CXCL11 levels are significantly (p = 0.0064 and p = 0.0017, respectively) elevated in those with stage > 2 compared to those with stage = 1. CXCL9 levels are also significantly (p = 0.0093) elevated in those with stage = 2 compared to those with stage = 1. The lower row of the box and whisker plots illustrate the expression levels of d) CXCL10, e) CXCL9, and f) CXCL11 among patients with chronic HCV infection stratified according to viral genotype. The Y-axis indicates the logarithmic-transformed levels for each chemokine as determined by real-time PCR. The number of patients per group is indicated in parenthesis. Patients with extreme values were the same for all three chemokines. Note different Y-axis values between CXCL10 and CXCL9/CXCL11.