| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Research Abstract |
Immunosuppressive cell types, which physiologically down-regulate excessive immune responses, hamper the development of effective anti-tumor immunity. CD11b^+Gr-1^+ immature myeloid suppressor cells (MSCs) increase in mice bearing various types of cancers, and have been shown to suppress anti-tumor T cell responses by several mechanisms. Thus, measures that inhibit the function of MSCs are important to enhance anti-tumor immune responses.
Initially, we observed that type I interferon (IFN-α/β) reversed the suppressive effect of MSCs from CT26 (colon cancer cell line)-bearing BALB/c mice on T cell proliferation. Since exposure of MSCs but not T cells to IFN-β was sufficient to reverse the suppressive effect of MSCs, IFN-β was likely to directly act on MSCs.
During experiments, however, we became unable to observe the increase in MSCs in tumor-bearing mice. Furthermore, after overcoming this problem, we became unable to observe the reversal of the immunosuppressive effect of MSCs by type I IFN. Therefore, we conclude that our initial observation that type I IFN diminishes the immunosuppressive effect of MSCs is not a physiologically meaningful, reproducible phenomenon. The reason why we initially observed the suppressive effect of type I IFN on MSCs is unknown.
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