| Budget Amount *help |
¥18,200,000 (Direct Cost: ¥14,000,000、Indirect Cost: ¥4,200,000)
Fiscal Year 2011: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2010: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2009: ¥9,880,000 (Direct Cost: ¥7,600,000、Indirect Cost: ¥2,280,000)
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| Research Abstract |
Despite the advent of an age when "malignant" leukemia is cured by bone marrow transplantation, "benign" inflammatory bowel diseases(IBD) are still intractable lifelong diseases. We showed that immune memory T cells that remember the disease are formed in IBD, and perceiving them as "benign T-cell leukemia"-like lifelong pathology that spreads throughout the body, We demonstrated that interleukin-7(IL-7) and commensal bacteria are essential as a survival factor for the maintenance and proliferation of colitogenic CD4^+memory T cells, in IBD. Although IL-17A is thought to be preferentially produced by T_h17 cells and to play a critical role in autoimmune disease development, it seems to inhibit development of T_h1 cells in some circumstances. Colitogenic T_h1 cells and T_h17 cells seem to interfere with each other in vivo under inflammatory conditions. At least in inflammatory conditions, colitogenic T_h1 cells and T_h17 cells are not independently generated ; rather the linear sequential developmental pathway from T_h17 to Th1 cells seems to dominate. Further study is needed to determine whether the classical T_h1 cells directly generated from naive T cells in an RORγt-independent manner are also involved in IBD pathogenesis. The pathway from T_h17/T_h1 cells to alternative T_h1 cells is suppressed by T_<reg> cells, resulting in the accumulation of T_h17 cells by T_<reg> cells.
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