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Optimal activation of T cells requires second costimulatory signals together with the first signal delivered by engagement of the T‑cell receptor with the peptide‑MHC complex on antigen presenting cells (APCs such as macrophages B cells and dendritic cells. The interaction between B7 molecules i.e. B7‑1 (CD80B7‑2 (CD86 on APCs and CD28CTLA‑4 molecules on T cells is the most well‑characterized costimulatory signal pathway and is thought to be crucial in eliciting an antitumor immune response. Recently several new members of the B7 family B7‑H1 B7‑H2 B7‑H3 and B7‑H4 have been identified. B7‑H1 inhibits the proliferation of T cells through a counterreceptor programmed death 1 (PD‑1 and delivers a stimulatory signal to T cells through an as yet unidentified counterreceptor other than PD‑1 12 . We detected the expression of B7‑H1 on activated T cells and some tumor cells such as those from melanoma lung ovarian and colon cancers and showed that B7‑H1 on tumor cells suppresses antitumor immunity by inhibiting the proliferation of tumor‑specific cytotoxic T lymphocytes (CTLs 3 . Consistent with these results patients with renal cell carcinoma and breast cancer expressing B7‑H1 have been reported to have a poor prognosis. B7‑H2 is expressed on professional APCs and tumor cells such as those from glioma and gastric carcinoma. The counterreceptor of B7‑H2 inducible costimulator (ICOS is expressed on activated T cells. The B7‑H2‑ICOS signal induces T cells to proliferate and to secrete both Th1 and Th2 cytokines such as interleukin (IL‑4 and interferon‑γ but not the potent Th1 cytokine IL‑2. Furthermore the B7‑H2‑ICOS signal induces IL‑10 production. When we investigated the expression of B7 family molecules in hematological malignancies B7‑H1 or B7‑H2 or both were detected in leukemia myeloma and lymphoma cells. We have recently reported that cells from many patients with acute myeloid leukemia (AML express B7‑2 and B7‑H2 molecules and that B7‑1 and B7‑H1 expression is rare 4 . Patients with B7‑H2‑positive AML had significantly shorter survival times. Furthermore B7‑ 2 expression was associated with hyperleukocytosis. Consistent with these findings AML cells expressing B7‑2 and B7‑H2 induced allogeneic CD4 + T cells to proliferate and secrete IL‑4 and IL‑10 in vitro effects that were

Expression and Function of B7 Family Molecules on Blasts of Patients with Myelodysplastic Syndromes