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存在疾病亚群。并试图描述这些疾病亚群（Arthritis Rheum, 31:37, 1988）。我们研究了与严重疾病亚群相关的基本细胞学差异，发现严重RA患者关节附近的骨骺骨髓中存在异常髓样细胞，而相应的正常和非RA骨髓中不存在异常髓样细胞（J Rheumatol, 15:1509, 1988）。在同一病变中，发现特别高滴度的髓细胞生长因子活性（见新闻）。然后，我们研究了多形核中性粒细胞（PMN），骨髓系细胞的发育细胞。积聚在病变部位的PMN表现出对组织破坏的特殊活性（生物医学研究，9:39 5,1988），PMN因子活性最初是由Nagai博士的小组在胶原诱导的大鼠中发现的。由于骨髓可能是产生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，细胞因子活性应该在炎症最重要的病变中被激活，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的活性升高伴随着骨髓的组织学改变（生物医学研究，1988）。我们认为这些异常的骨髓细胞级联和骨髓病变在类风湿关节炎的病理机制中起着重要的作用，并正在对此进行更多的研究。

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.