IMMUNOREGULATORY MECHANISMS IN THE RHEUMATIC DISEASES

这项建议的长期目标是加深对 调节和调节人类免疫反应的细胞成分。 我们计划识别、描述和寻找新描述的异常 慢性阻塞性肺疾病患者血液和组织中发现的单个核细胞亚群 风湿病。我们将继续研究“L”细胞，一个假定的子集 对IGC具有高亲和力的非T、非B细胞的Fc受体。精准的 L细胞与其他单个核细胞的关系将通过 L细胞等单核细胞表面抗原的鉴定 杂交瘤产生的单抗。流式细胞荧光造影术将 用来完成这项任务的。其次，特定的细胞类型将是 根据细胞表面标记通过细胞分选和 纯化细胞的功能特性将在体外进行比较 技巧。我们将研究L细胞-T细胞在调节过程中的相互作用 B细胞功能。第三，L细胞是自发性OR的良好介体。 自然杀伤抗体依赖的细胞细胞毒性。两个版本之间的比较 L细胞与其他细胞类型的细胞毒作用将继续存在。最后， 我们计划了解一种细胞毒性缺陷的重要性 最近被描述为类风湿性关节炎。将进行研究，以确定 参与这一缺陷的效应细胞和调节细胞，以了解 这种缺陷是否可能是类风湿的重要致病因素 关节炎，并研究纠正这一缺陷的可能方法。它是 很可能对慢性阻塞性肺疾病患者的调节异常有更好的了解 风湿病将导致控制这些疾病的新的、更安全的方法 精神错乱。

The long-term objective of this proposal is to develop a greater understanding of the cellular components which mediate and regulate the human immune response. We plan to identify, characterize and look for abnormalities of newly described subsets of mononuclear cells found in the blood and tissues of patients with rheumatic diseases. We will continue to study "L" cells, a presumptive subset of non-T, non-B cells with high avidity Fc receptors for IgC. The precise relationship of L cells with other mononuclear cells will be investigated by characterizing cell surface antigens on L cells and other mononuclear cells with monoclonal antibodies produced by hybridomas. Flow cytofluorography will be utilized to accomplish this task. Secondly, specific cell-types will be separated on the basis of cell surface markers by cell-sorting and the functional properties of purified cells will be compared using in vitro techniques. We will investigate L cells-T cells interactions in the regulation of B cell function. Thirdly, L cells are excellent mediators of spontaneous or natural killer antibody-dependent cellular cytotoxicity. A comparison of the cytotoxic effects of L cells with other cell types will be continued. Finally, we plan to learn the significance of a cellular cytotoxicity defect we have recently described in rheumatoid arthritis. Studies will be conducted to define the effector cells and regulatory cells involved in this defect, to learn whether this defect may be an important pathogenetic factor in rheumatoid arthritis and to investigate possible means of correcting this defect. It is likely that a better understanding of regulatory abnormalities in patients with rheumatic diseases will lead to new and safer approaches to control these disorders.