| Budget Amount *help |
¥64,350,000 (Direct Cost: ¥49,500,000、Indirect Cost: ¥14,850,000)
Fiscal Year 2013: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2012: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2011: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2010: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2009: ¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
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| Research Abstract |
In our research, we demonstrated in in vitro experiments that blockade of CD26-mediated T cell costimulation by soluble Fc fusion proteins containing the N-terminal domain of caveolin-1 (Cav-Ig) diminished primary and secondary proliferative responses not only to recall antigen, but also to unrelated allogeneic antigen-presenting cell. To expand the in vitro findings to an in vivo system, we examined CD26-dependent organ injury in a xenogeneic GVHD (xGVHD) murine model. Administration of humanized anti-human CD26 monoclonal antibody (mAb) decreased xGVHD severity and prolonged survival in hu-PBL-NOG mice without loss of engraftment of human T cells, while increasing doses of CTLA4-Ig diminished engraftment of human lymphocytes. Importantly, anti-CD26 mAb treatment preserved the graft-versus-leukemia effects. Altogether, our findings indicate a role for CD26 in the regulation of GVHD and point to CD26 as a novel target for therapeutic intervention in this disease.
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