Fig. 4
EVs shed by renal cancer cells inhibited monocyte-derived DC differentiation and their ability to stimulate T cell proliferation. a Mean percentage expression ± SD of CD80, CD86, HLA-DR, CD1a, α4 integrin, CD54, α5 integrin, CD14, CD83 and CD40 by monocyte-derived DCs differentiated in the presence or in absence (CTL DC) of CD105+ EVs (CD105+ EV Mo) or CD105- EVs (CD105- EV Mo). Results were obtained from 6 independent experiments. ANOVA with Newman Keuls multicomparison test was performed: *p < 0.05 CD105+ EV Mo and CD105- EV Mo versus CTL DC; § p < 0.05 CD105+ EV Mo versus CD105- EV Mo. b MFI ± SD of CD83, CD40, α5 integrin CD80, CD86, HLA-DR and CD54 of monocyte-derived DCs differentiated in the presence or in absence (CTL DC) of CD105+ EVs (CD105+ EV Mo) or CD105- EVs (CD105- EV Mo). Results were obtained from 6 independent experiments. ANOVA with Newman Keuls multicomparison test was performed: *p < 0.05 CD105+ EV Mo and CD105- EV Mo versus CTL DC; § p < 0.05 CD105+ EV Mo versus CD105- EV Mo. c Monocyte-derived DCs differentiated in the presence or in absence (CTL DC) of CD105+ EVs (CD105+ EV Mo) or CD105- EVs (CD105- EV Mo) were plated at cell concentration of 2x104 with 1x105 T CD3+ lymphocytes. Forty eight hours later T-cell proliferation was assessed. Data are expressed as mean ± SD of percent variation of T-cell proliferation in the presence of DCs differentiated in the presence of renal cancer cells in respect to T-cell proliferation in presence of DCs matured in the absence of EVs (established as 100 %). Results were obtained from 4 independent experiments. ANOVA with Newman Keuls multicomparison test was performed: *p < 0.05 CD105+ EV Mo versus all the other conditions