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. 2008 Nov 8;58(6):887–900. doi: 10.1007/s00262-008-0605-3

Fig. 1.

Fig. 1

Tumour antigen-reactivity of bone marrow T cells from metastasized breast cancer patients. a Activated DC phenotype after pulsing with tumour cell lysate. Generated DC were pulsed with tumour lysate for 24 h and phenotyped by flowcytometry. Left dot plot CD11c expression of gated, viable (PI-) lineage marker-DC. Right panel Expression of HLA-Dr, CD40, CD80 and CD83 on gated DCs (black lines). Isotype controls are shown as grey lines. b, c IFN-γ ELISPOT assay of bone marrow T cell from one HLA-A0201+ patient (who was not included into the study) with reactivity against HLA-A2-restricted peptides from the tumour antigens MUC1, Her-2/neu and heparanase (b) and tumour antigens derived from MCF-7 breast cancer cells (c). Mean values and SD of triplicate wells containing tumour antigens (black bars) or control antigens (b irrelevant control peptide HLVEALY LV, c U937-lysate, white bars) are shown. Asterisk Significant difference between test and respective control wells P < 0.05, Student’s T-test). d Frequencies of MCF-7-specific type-1 T cells in bone marrow of breast cancer patients as determined by IFN-γ-ELISPOT-analysis (P < 0.05 compared to negative control wells containing U937 lysate, Student’s T-test). Black squares patients who were included into the study, white squares patients excluded from study treatment. The numbers (Px) indicate different study patients. e Scheme of treatment preparation