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©2012 Baishideng Publishing Group Co.
World J Gastroenterol. Jul 28, 2012; 18(28): 3681-3695
Published online Jul 28, 2012. doi: 10.3748/wjg.v18.i28.3681
Published online Jul 28, 2012. doi: 10.3748/wjg.v18.i28.3681
Figure 7 In vitro kinetic analysis of CD40 and human B7 homolog 1 expression on myeloid dendritic cells, with or without hepatitis B surface antigen pretreatment, stimulated by poly (I:C).
A: The FSC and SSC of myeloid dendritic cells (mDCs) with r hepatitis B surface antigen (HBsAg) pretreatment were not altered significantly compared to those without rHBsAg pretreatment. This result suggests that the vitality of mDCs with or without HBsAg pretreatment is similar; B: Representative plots of CD40 and B7 homolog 1 (B7-H1) expression on mDCs with or without HBsAg pretreatment. Values in the upper right quadrant indicate the percentage of CD40 or B7-H1 positive cells; C: With HBsAg pretreatment, the percentage of CD40 (left) and B7-H1 (right) positive cells within mDCs were decreased significantly at 16 h, 20 h and 24 h time points (for CD40, aP < 0.05 at 16 h, 20 h and 24 h time point; for B7-H1, cP < 0.05 at 16 h and 24 h time point, n = 10); D: With HBsAg pretreatment, the MFI of CD40 (left) and B7-H1 (right) were decreased significantly at 16 h and 20 h time points ( for CD40 and B7-H1, aP < 0.05 at 16 h, 20 h and 24 h time point, n = 10); E: The inhibition rate was calculated using following equation: 1-MFI of CD40 or B7H1 with HBsAg pretreatment/MFI of CD40 or B7H1 without HBsAg pretreatment. The results showed that at 8 h, 16 h, 20 h and 24 h time point, the inhibition rate of CD40 was greater significantly than that of B7H1 (P < 0.05 at 8 h time point, P < 0.01 at 16 h time point, P < 0.05 at 20 h time point, P < 0.01 at 24 h time point). MFI: Mean fluorescence intensity; FSC: Forward scatter; SCC: Side scatter.
- Citation: Zhang WJ, Xie HY, Duan X, Wan YL, Peng CH, Shi SH, Su R, Zheng ZH, Pan LL, Zhou L, Zheng SS. Study of human B7 homolog 1 expression in patients with hepatitis B virus infection. World J Gastroenterol 2012; 18(28): 3681-3695
- URL: https://www.wjgnet.com/1007-9327/full/v18/i28/3681.htm
- DOI: https://dx.doi.org/10.3748/wjg.v18.i28.3681