MECHANISMS OF HUMAN IN VITRO CELLULAR IMMUNE RESPONSES

我们过去两年的工作使我们认识到， 抗原非依赖性粘附是T细胞的关键早期事件， 淋巴细胞与其他细胞的相互作用， 这种相互作用有两种分子途径 发生：T细胞CD 2（T11，E-玫瑰花结受体）与其 配体LFA-3和T细胞LFA-1与未知分子相互作用 配体。 今年的工作证实并扩展了这些 理念的 纯化的CD 2和LFA-3的生化研究表明， 他们彼此之间的联系，证实了我们的 基于功能研究的推断，LFA-3是 CD2。 一个特别有趣的例子， 这两条途径是里德的自发玫瑰花结 斯滕贝格细胞与人外周血T细胞。 此外，LFA-3已被证明是红细胞配体 其介导自体玫瑰花结。 二的概念 粘附途径已被扩展，以表明其相关性 T细胞介导的细胞毒性（CML）以及结合物 阵 慢性粒细胞白血病以及粘附的研究表明， ICAM-1是T细胞中LFA-1的主要配体， 细胞与某些靶点的相互作用，但表明其他靶点 未鉴定的配体参与与其它配体的相互作用。 目标的 由于这些粘附的功能重要性， 分子，我们仔细研究了它们在 外周血T细胞 我们的研究表明， LFA-3、CD 2和LFA-1的表达在一个主要的 外周血T细胞具有记忆功能 细胞，并提高这种增强表达的可能性， 这些功能重要的分子可能有助于 增强记忆T细胞的反应性。

Our work in the last two years has led to the realization that antigen-independent adhesion is a critical early event in T lymphocyte interactions with other cells, and we hypothesized that there are two molecular pathways by which such interactions occur: T cell CD2 (T11, E-rosette receptor) interacting with its ligand LFA-3 and T cell LFA-1 interacting with an unknown ligand. This year's work has confirmed and extended those concepts. Biochemical studies of purified CD2 and LFA-3 have confirmed the binding of each to the other -- corroborating our inference based on functional studies that LFA-3 is the ligand for CD2. A particularly interesting example of adhesion mediated by these two pathways is the spontaneous rosetting of Reed- Sternberg cells with human peripheral blood T cells. Furthermore, LFA-3 has been shown to be the erythrocyte ligand which mediates autologous rosetting. The concept of two pathways of adhesion has been extended to indicate its relevance to T-cell mediated cytotoxicity (CML) as well as conjugate formation. Studies of CML as well as adhesion demonstrate functionally that ICAM-1 is the principal ligand for LFA-1 in T cell interaction with some targets, but suggest that other as yet unidentified ligands are involved in interactions with other targets. Because of the functional importance of these adhesion molecules, we have carefully investigated their expression on peripheral blood T cells. Our studies demonstrate that expression of LFA-3, CD2, and LFA-1 is increased on a major subset of peripheral blood T cells with the functional properties of memory cells and raise the possibility that such enhanced expression of these functionally important molecules may contribute to the enhanced responsiveness of memory T cells.