Figure 2. Host miR-155 deficiency enhances antigen-specific antitumor T cell immunity.

(A) Percentage and absolute number of CD4⁺CD3⁺, CD8⁺CD3⁺, Gr1⁺CD11b⁺, CD3⁻CD19⁺ and CD49b⁺NK1.1⁺ cells in tumor infiltrates of WT or miR-155^−/− mice collected 21 days after inoculation with EG7 tumor cells (n=5). (B) CD8⁺IFN-γ⁺ T cell frequency in spleen, DLN and tumor from EG7-bearing WT or miR-155^−/− mice 21 days after tumor inoculation (n=3–6). (C) Representative flow cytometric analysis of tumor antigen-specific CD8⁺ T cells from EG7-bearing WT or miR-155^−/− mice. Frequency of tetramer⁺ cells specific for the OVA epitope SIINFEKL in CD8⁺ infiltrates from mice in B, was summarized. (D) Representative flow cytometric analyses of in vivo antigen-specific killing capacity of antitumor T cells from EL4- or EG7-bearing WT and miR-155^−/− mice. Equal numbers of eFluor® 450^high SIINFEKL peptide-pulsed and eFluor® 450^low SIY–peptide-pulsed WT splenocytes were adoptively transferred into tumor-bearing mice. Numbers denote percentage of SIINFEKL peptide-pulsed target cell killing in DLN. Percent killing for EG7-bearing mice in DLN was calculated as described in Methods (n=3). (E) In miR-155^−/− mice (n= 5), depletion of CD4⁺ T cells, CD8⁺ T cells, or NK cells was achieved by twice weekly i.p. injection of control Ig, anti-CD4, anti-CD8, or anti–NK1.1 depleting Abs, respectively, beginning 1 day prior to tumor challenge. Data are representative of 2 independent experiments. *, p< 0.05; **, p<0.01.