IMMUNOLOGY OF CUTANEOUS HYPERSENSITIVITY

通过对皮肤嗜碱性粒细胞超敏反应（CBH）的研究， 嗜碱性粒细胞和肥大细胞，它们所含的介质（如组胺 和血清素）及其相关的过敏性抗体（IgE和 IgG 1）参与延迟时间过程反应。 这些发现意味 过敏性疾病和哮喘中重要的免疫成分也 在对微生物和寄生虫的免疫抵抗中以及在 肿瘤和组织移植物的排斥反应。 本研究报告提出了一个 继续调查的作用的综合方案 豚鼠CBH反应中的抗体。 我们会研究有关机制， 这些抗体介导CBH通过确定是否循环 嗜碱性粒细胞和到达CBH反应的嗜碱性粒细胞被致敏， 转移CBH的抗体 我们还将确定这些 抗体是IgG 1的一个特殊亚类，无论是淋巴细胞还是 巨噬细胞参与抗体介导CBH的能力。 最后，将进行研究，以确定这些抗体是否 也参与CBH反应，通过胸腺衍生的 淋巴细胞（T细胞）。 还将继续研究 T细胞激活肥大细胞释放血管活性胺 血清素在小鼠迟发型超敏反应（DTH）中的作用。 血清素 从肥大细胞在DTH中的转运，并在体外进行研究。 桅杆 细胞来源的血清素蛋白，可能在运输中很重要 5-羟色胺将被表征。 最后，我们将确定机制 通过确定T细胞是否可以激活DTH中的肥大细胞， 非特异性5-羟色胺释放淋巴因子或特异性IGF样因子 参与其中

Through study of cutaneous basophil hypersensitivity (CBH) it is now clear that basophils and mast cells, their contained mediators (such as histamine and serotonin), and their associated anaphylactic antibodies (IgE and IgG1), are involved in delayed-time course reactions. These findings mean that immune components improtant in allergic disease and astha are also potentially important in immune resistance to microbes and parasites and in rejection of tumors and tissue grafts. This research proposal submits a comprehensive program for the continued investigation of the role of antibodies in CBH responses of guinea pigs. We will study the mechanism by which these antibodies mediate CBH by determining whether circulating basophils, and basophils arriving at CBH reactions are sensitized with antibodies that transfer CBH. We will also determine whether these antibodies are a special subclass of IgG1 and whether lymphocytes or macrophages are involved in the ability of antibodies to mediate CBH. Finally, studies will be performed to determine whether these antibodies are also involved in CBH reactions that are transferred by thymic-derived lymphocytes (T cells). Studies will also be continued on the requirement for T cells to activate mast cells to release the vasoactive amine serotonin in murine delayed-type hypersensitivity (DTH). Serotonin transport from mast cells in DTH, and in vitro will be studied. A mast cell-derived serotonin protein that may be important in transport of serotonin will be characterized. Finally, we will determine the mechanism by which T cells may activate mast cells in DTH by determining whether non-specific serotonin releasing lymphokines, or specific IgF-like factors are involved.