| Budget Amount *help |
¥7,100,000 (Direct Cost: ¥7,100,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1986: ¥3,600,000 (Direct Cost: ¥3,600,000)
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| Research Abstract |
Based on natural course of joint destruction and fluctuation of serum Clq levels. we showed the existence of disease subsets in RA. and tried to characterize these disease subsets (Arthritis Rheum, 31:37, 1988). We studied the fundamental cytological differences correlating to severer disease subsets, and found the presence of unusual myeloid cells in epiphyseal bone marrow adjacent ot joints affected with severe disease of RA and its absence in the corresponding normal and non-RA bone marrow (J Rheumatol, 15:1509, 1988). In the same iesion, especially high titer of myeloid cell growth factor activity was found (in press). Then, we studied about polymorphonuclear neutrophiles (PMN), developped cells of myeloid lineage cells.
PMN accumurating in that lesion showed special activity for tissue destruction (Biomedical Research, 9:395, 1988), PMN factor activity, originally found in collagen-induced rat by Dr. Nagai's group. As bone marrow could be important lesion to produce polyarthritis, we tried to contirm this hypothesis by cytokine activities, which should be activated in the most important lesionfor inflammation, but had not yet clearly found in vivo. In collageninduced rats, we found elevated activities of interleukines in thebone marrow accmpanying the histological changes in the bone marrow (Biomedical Research 9:401, 1988). We believe the important roles of theseabnormal myeloid cell cascade and the bonemarrow lesions in the pathomechanisms of RA, and are studying more about these.
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