| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Research Abstract |
In some proportions of the patients with inflammatory bowel disease, unresponsiveness to glucocorticoid, which is one of the major therapeutic drugs for the disease, are noted during the course. We have reported that the nonfunctional isoform of the intracytoplasmic glucocorticoid receptor, namely hGR beta was expressed in peripheral blood mononuclear cells in glucocorticoid-resistant patients with IBD. In this process, proinflammatory IL-7 and IL-18 may augments hGR beta mRNA synthesis. In this study, we purposed to clarify the mechanism of glucocorticoid resistance in lymphocytes by measuring the size of IL-18-receptor-bearing lymphocytes and hGR beta mRNA expression in these cells, as a marker for clinical refractoriness. Until now, we have found the serum IL-18 concentration and hGR beta mNRA expression was positively correlated. We could not see the correlation between populations of IL-18 receptor positive T lymphocyte and patients responsiveness to glucocoticoid, or hGR beta mRNA expression. Leukocyteapheresis using extracorporeal circulation by centrifugal cell separator, or leukocyte absorbing filters, which reduced the disease activity of IBD, did not alter the hGR beta expression. Further investigation to elucidate the mechanisms glucocorticoid unresponsive of T lymphocyte, especially to find the role of hGR beta inducing IL-18 should be performed
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