A myeloid cell population showing oncofetal membrane marker found in epiphyseal bone marrow adjacent to joints affected with rheumatoid arthritis.

基于关节破坏的自然过程和血清Clq水平的波动。我们发现RA中存在疾病亚群。并试图表征这些疾病亚群（Arthritis Rheum，31：37，1988）。我们研究了与较严重的疾病亚群相关的基本细胞学差异，发现在受严重RA疾病影响的关节附近的骺骨髓中存在异常的髓样细胞，而在相应的正常和非RA骨髓中不存在（J Rheumatol，15：1509，1988）。在同一病变中，还发现了特别高滴度的髓样细胞生长因子活性（出版中）。然后，我们研究了多形核嗜中性粒细胞（PMN），即髓系细胞的发育细胞，在该病变中的PMN增殖显示出对组织破坏的特殊活性（Biomedical Research，9：395，1988），PMN因子活性，最初由永井博士的小组在胶原诱导的大鼠中发现。由于骨髓可能是多发性关节炎的重要病变，我们试图通过细胞因子活性来证实这一假设，这些细胞因子应在炎症的最重要病变中被激活，但在体内尚未明确发现。在胶原诱导的大鼠中，我们发现骨髓中白细胞介素活性升高，与骨髓中的组织学变化一致（Biomedical Research 9：401，1988）。我们认为这些异常的骨髓细胞级联反应和骨髓病变在RA的发病机制中起着重要作用，并对其进行了进一步研究。

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.