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. Author manuscript; available in PMC: 2015 May 15.
Published in final edited form as: J Immunol. 2014 Apr 9;192(10):4748–4757. doi: 10.4049/jimmunol.1303190

Figure 4. Expression of MHC II on LC treated with wildtype HPV16 or L2 mutant HPV16 PsV.

Figure 4

A. LC were either left untreated (grey lines), treated with LPS, HPV16 wild-type (WT) PsV, or HPV16 L2 mutant PsV (black lines). After 48 hr, the cell surface expression of MHC II was and analyzed by flow cytometry. The HPV16 L2 mutant PsV and LPS caused phenotypic activation of LC compared to untreated cells while there was a slight decrease in MHC II expression in WT HPV16PsV treated LC. Isotype controls are shown as grey dotted lines B. The mean fluorescent intensity (MFI) of MHC II-FITC stained cells was 624 for WT PsV and 837 for HPV16 L2 mutant PsV with p = 0.04 as determined by a two-tailed, unpaired t-test, for the means of 3 independent experiments. C. LC were either left untreated, treated with LPS, HPV16 WT PsV, or HPV16 L2 mutant PsV. After 48 hr, the cell surface expression of CD86 was and analyzed by flow cytometry. The HPV16 L2 mutant PsV caused a significantly greater expression of CD86 compared to WT HPV16 VLP (p<0.05 as determined by a two-tailed, unpaired t-test, for the means of 3 independent experiments).