Fig. 1
Renal cancer cells suppressed monocyte-derived DC differentiation and their ability to stimulate T cell proliferation. a Mean percentage expression ± SD of CD14, CD83, α5 integrin, CD40, α4 integrin, CD80, CD86, HLA-DR, CD1a and CD54 by monocyte-derived DCs differentiated in the presence or in absence (CTL DC) of CD105+ CSCs (CD105+ Mo) or CD105- TCs (CD105- Mo). Results were obtained from 6 independent experiments. ANOVA with Newman Keuls multicomparison test was performed: *p < 0.05 CD105+ Mo and CD105- Mo versus CTL DC; § p < 0.05 CD105+ Mo versus CD105- Mo. b MFI ± SD of CD14, CD83, CD80, CD40, α4 integrin, CD54, α5 integrin, CD86, HLA-DR and CD1a of monocyte-derived DCs differentiated in the presence or in absence (CTL DC) of CD105+ CSCs (CD105+ Mo) or CD105- TCs (CD105- Mo). Results were obtained from 6 independent experiments. ANOVA with Newman Keuls multicomparison test was performed: *p < 0.05 CD105+ Mo and CD105- Mo versus CTL DC; § p < 0.05 CD105+ Mo versus CD105- Mo. c Monocyte-derived DCs differentiated in the presence or in absence (CTL DC) of CD105+ CSCs (CD105+ Mo) or CD105- TCs (CD105- 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 presence of renal cancer cells in respect to T-cell proliferation in presence of DCs matured in the absence of cells (established as 100 %). Results were obtained from 5 independent experiments. ANOVA with Newman Keuls multicomparison test was performed: *p < 0.05 CD105+ Mo versus all the other conditions