Synergistic effects of antiplatelet therapy and IC inhibition in experimental breast cancer. (A) Surface expression of CD80, CD86, PD-L1, PD-L2, CD40, and CD40L on phosphatidylserine^low or phosphatidylserine^high platelets from the peripheral blood of mice; quantitative data are shown (mean ± SEM for n = 3 mice per group; ∗P < .05 vs phosphatidylserine^low). (B) Activation status of platelet-bound (CD41⁺) or -unbound (CD41⁻) lymphocytes isolated from orthotopically raised 4T1 tumors as assessed by L-selectin/CD62L surface expression by flow cytometry, and quantitative data are shown (mean ± SEM for n = 3 mice per group). (C) Activation status of platelet-bound (CD41⁺) lymphocytes, as assessed by L-selectin/CD62L surface expression in flow cytometry upon antibody blockade of CD80, CD86, CTLA4, PD-L1, or PD-1, quantitative data are shown (mean ± SEM for n = 3 mice per group). (D) Infiltration by neutrophils, cMOs, B cells, CD8⁺ T cells, and CD4⁺ T-cell subsets of orthotopic 4T1 tumors in mice receiving anti-PD-1 and -CTLA4 monoclonal antibodies (mAbs) or isotype control antibodies as assessed by flow cytometry; quantitative data are shown (mean ± SEM for n = 5 mice per group; ∗P < .05 vs isotype control). (E) Relative volume and weight of tumors as well as (F) relative infiltration by lymphocytes and myeloid leukocytes of orthotopically grown 4T1 tumors in mice receiving anti-GPIbα mAbs, and/or anti–PD-1 and -CTLA4 mAbs, or isotype control antibodies; quantitative data are shown (mean ± SEM for n = 5 mice per group; ∗P < .05 vs isotype control).