LYMPHOCYTE ADHERENCE IN MULTIPLE SCLEROSIS

多发性硬化症(MS)是一种慢性中枢脱髓鞘疾病 神经系统。很可能紊乱的免疫机制和/或 炎症反应的调节缺陷是导致 导致MS组织损伤的病理过程。 前列腺素(PGs)及花生四烯酸的其他产物(C20：4) 新陈代谢是细胞功能的重要调节因素，也是 发炎。虽然证据是模棱两可的，PG对免疫的调节 MS患者的功能可能发生改变。我们已经表明，增加了 MS患者的淋巴细胞黏附(病毒感染的细胞和髓鞘)可能 是由于单核细胞依赖，前列腺素E介导的机制和 MS单核细胞自发地在组织中产生更高水平的PGE 文化。因此，淋巴细胞粘附性的增加可能是在体外 单核细胞控制的前列腺素E调节T细胞反应的测量 (坚持)。有可能PG介导的调节或控制 淋巴细胞表面受体可以在一定程度上解释 在多发性硬化症中观察到的免疫副现象我们将继续描绘 控制淋巴细胞与髓鞘黏附的机制，并将评估 外周血单核细胞、单核细胞功能与花生四烯酸 尤其是MS的代谢，这些研究将包括对 MS单核细胞、脑脊液白细胞及其受体花生四烯酸代谢的研究 淋巴细胞与髓鞘黏附的关系。结果将相互关联 具有临床特征。此外，作为我们研究的延伸，我们将 检测单核细胞功能、Ia抗原表达及单核细胞的作用 在淋巴细胞黏附方面。这些研究很可能会提供 单核细胞-前列腺素相互作用及其机制的新信息 在多发性硬化症白细胞功能改变中的作用。

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. It is likely that disordered immune mechanisms and/or defective regulation of inflammatory responses are central to the pathological processess which result in tissue injury in MS. Prostaglandins (PGs) and other products of arachidonic acid (C20:4) metabolism are important regulators of cell function and local mediators of inflammation. While the evidence is equivocal, PG regulation of immune function may be altered in MS patients. We have shown that increased lymphocyte adherence (virus infected cells and myelin) in MS patients may be due to a monocyte dependent, and prostaglandin E mediated mechanism and that MS monocytes spontaneously produce increased levels of PGE in tissue culture. Thus, increased lymphocyte adherence may be in an in vitro measurement of a monocyte controled PGE modulation of a T-cell response (adherence). It is possible that PG-mediated modulation or control of lymphocyte cell surface receptors can, in part, account for much of the immunologic epiphenomena observed in MS. We will continue to delineate mechanisms which govern lymphocyte adherence to myelin and will evaluate peripheral blood monocytes, monocyte function and arachidonic acid metabolism in MS. In particular, these studies will include evaluation of arachidonic acid metabolism in MS monocytes, CSF leukocytes and their relation to lymphocyte adherence to myelin. Results will be correlated with clinical features. Further, as an extension of our studies, we will examine monocyte function, Ia antigen expression and the role of monocytes in lymphocyte adhesion. It is likely that these studies will provide useful new information on monocyte-prostaglandin interactions and their role in altered leukocyte function in multiple sclerosis.