| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Research Abstract |
We assessed the roles of ICOS and ICOSL in tissue fibrosis by administering bleomycin intratracheally or intradermally into ICOS and/or ICOSL-deficient mice. The loss of ICOS attenuated fibrosis of lungs and skin, whereas deficiency of ICOSL aggravated it. Mice deficient in both ICOS and ICOSL also exhibited accelerated fibrosis, reflecting a dominant role for ICOSL over ICOS in this model. ICOSL expression on macrophages and B cells in bronchoalveolar fluids was significantly elevated in ICOS-deficient mice compared to wild type mice during this process. Thus, ICOSL expression levels on B cells and macrophages were inversely associated with the severity of tissue fibrosis. Our results indicate that ICOSL expression on antigen presenting cells plays a previously unknown regulatory role during the development of bleomycin-induced tissue fibrosis which is independent of the ICOS-ICOSL pathway.
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