IMMUNOCHEMICAL STUDIES OF CHEMOATTRACTANT SUBSTANCES

化学引诱物物质的产生被认为是重要的 在感染和过敏过程的发展和结果中的作用。 最近的研究已经引起了人们对 例如LPC（溶血磷脂酰胆碱）、HETE（5-羟基或 12-羟基二十碳四烯酸）和衍生自 膜磷脂 因此，我们启动了免疫学 生物化学研究的目的是：（1）进一步开展 溶血磷脂酰胆碱的研究，一种新认识的化学引诱剂， 淋巴细胞，（2）研究补体诱导的新方面 通过评估补体蛋白C5 b-9在炎症中的作用， 产生LPC、HETE、白三烯，可能还有其他物质 来自膜磷脂的化学引诱物。 关于LPC，我们想要确定哪些细胞类型对其响应。 引诱剂活性，它在体内作为介体发挥什么作用， 炎症，LPC的结构类似物表现出化学引诱物 活性，LPC是否通过响应转化为其他化学引诱物 细胞，以及LPC是否可以诱导形成新的化学引诱物 包括一些花生四烯酸代谢物和已知的化学引诱物 活动 关于补体，我们想确定哪些细胞类型 当被C5 b-9攻击时产生化学引诱因子，并评估 LPC、HETE、白三烯和可能的其他物质的形成 化学引诱物 我们希望这些努力将扩大知识， 补体诱导的炎症超出了众所周知的活动， 补体片段C3 a、C4 a、C5 a和C3 b。 我们认为， 感染、过敏和恶性肿瘤组织部位的补体， 导致细胞膜损伤， 磷脂酶和其他有助于生产的酶 化学引诱剂磷脂衍生物，包括LPC。

Generation of chemoattractant substances is believed to play an important role in the development and outcome of infectious and allergic processes. Recent studies have attracted attention to chemoattractant activities of substances such as LPC (lysophosphatidylcholine), HETEs (5-hydroxy or 12-hydroxy eicosatetraeonic acid) and leukotrienes which are derived from membrane phospholipids. Accordingly, we have initiated an immunological and biochemical investigation with the purpose of: (1) Conducting further studies of lysophosphatidylcholine, a newly recognized chemoattractant for lymphocytes, and (2) investigating a new aspect of complement-induced inflammation by assessing the role of complement proteins C5b-9 in the generation of LPC, HETEs, leukotrienes and, possibly, other chemoattractants from membrane phospholipids. With respect to LPC we want to determine what cell types respond to its attractant activity, what role it plays in vivo as a mediator of inflammation, what structural analogs of LPC exhibit chemoattractant activity, whether LPC is converted to other chemoattractants by responding cells, and whether LPC can induce formation of new chemoattractants including some arachidonate metabolites with known chemoattractant activity. With respect to complement, we want to determine what cell types produce chemoattractant factors when attacked by C5b-9 and to assess formation of LPC, HETEs, leukotrienes and, possibly, other chemoattractants. We expect that these efforts will expand knowledge of complement-induced inflammation beyond the well-known activities of complement fragments C3a, C4a, C5a, and C3b. We believe that activation of complement at tissue sites of infection, allergy and malignancy, is likely to lead to membrane damage which could activate membrane-associated phospholipase and other enzymes that are instrumental in producing chemoattractant phospholipid derivatives, including LPC.