Molecular mechanisms of chronic inflammaroty proliferative disease

我们提出了一个疾病类别，应该被称为慢性炎症性增生性疾病（CIPD）。CIPD表现为1)慢性炎症，2)致病细胞慢性增殖，3)免疫应答参与，4)多基因表达失调。我们分析了类风湿关节炎（RA）中表达的基因产物，类风湿关节炎是典型的CIPD之一。我们从ra来源的骨髓基质细胞中分离出新的细胞表面分子BST-1和BST-2。我们发现某些严重RA患者血清中有大量可溶性BST-1。我们对RA中IL-6表达失调的分子机制的研究尚未成功，但我们发现人细小病毒产物可以通过NF-kappaB诱导IL-6基因的表达。我们还阐明了另一种参与CIPD的分子白介素6的分子机制。我们的研究表明JAK-STAT信号转导通路在细胞生长和存活中起着至关重要的作用。

We have proposed a disease category which should be called as chronic inflammatory proliferative disease (CIPD). CIPD shows 1) chronic inflammation, 2) chronic proliferation of pathogenic cells, 3) involvement of immune response and 4) deregulated expression of multiple genes. We have analyzed gene products expressed in rheumatoid arthritis (RA), one of typical CIPD.We isolated novel cell surface molecules, BST-1 and BST-2 from RA-derived bone marrow stromal cells. We showed that certain severe RA patients have a large amount of soluble BST-1 in sera. Our trial to identify the molecular mechanisms which are involved in the deregulated expression of IL-6 in RA has not been successful, but we showed that human parvovirus product can induce IL-6 gene expression through NF-kappaB.We also elucidated the molecular mechanisms of interleukin 6, another molecule involved in CIPD.Our study showed that JAK-STAT signal transduction pathway plays critical roles in cell growth and survival.