M CELL UPTAKE AND CYTOARCHITECTURE IN PEYER'S PATCHES

我们的目标是界定的职能和监管 肠道淋巴器官。这些目标与口语有关 免疫、肠道感染、M细胞抗原摄取和 颗粒，包括HTLV III，与免疫学发病机制 疾病。 第一个具体目标是定义对 微粒微生物抗原、示踪剂颗粒和脂质体 动物模型。我们建议研究衣原体的进入途径(S) 通过小肠和直肠淋巴滤泡的微生物 上皮细胞和这些微生物的转运机制 淋巴组织。衣原体感染的后果 淋巴滤泡增生对M细胞增殖的影响 将评估流明颗粒的摄取情况。调制方式 分泌型IgA将从肠腔摄取抗原 使用霍乱弧菌进行评估，并使用和 不含IgA抗体。含有~3H标记蛋白的脂质体或 胶体金颗粒将用于评估口服给药 通过M细胞传递抗原和药物。的迁移路径 单核白细胞将被追踪以确定细胞 可以将抗原从肠腔带入Peyer‘s补片。 第二个具体目标是研究Peyer的调制 抗原刺激的补片细胞结构和功能 通过耗尽正常小鼠和小鼠的调节性淋巴细胞亚群 在系统性红斑狼疮(SLE)的小鼠模型中。这个 肠道抗原刺激调节的机制 Peyer‘s斑块的表面Ig同型转换将被评估 通过免疫标记和荧光激活细胞分选(FACS)。 单抗将用于清除淋巴细胞亚群； 免疫调节细胞的后续变化对血管内皮细胞生长的影响 粘膜淋巴器官的细胞结构将通过以下方法评估 正常小鼠和自身免疫性小鼠的免疫标记 辅助性T细胞耗竭治疗SLE。

Our objectives are to define the functions and regulation of intestinal lymphoid organs. These goals are relevant to oral immunization, intestinal infection, M cell uptake of antigens and particles, including HTLV III, and to pathogenesis of immunologic diseases. The first specific aim is to define uptake and transport of particulate microbial antigens, tracer particles, and liposomes in animal models. We propose to study the entry route(s) of chlamydia organisms through small intestinal and rectal lymphoid follicle epithelia and the mechanism of transport of these organisms into lymphoid tissues. The consequences of chlamydia-induced hyperplasia of lymphoid follicles on M cell proliferation and uptake of luminal particles will be evaluated. Modulation of antigen uptake from the intestinal lumen by secretory IgA will be assessed using cholera vibrios and also microspheres with and without IgA antibody. Liposomes containing 3H labeled proteins or colloidal gold particles will be used to evaluate peroral delivery of antigens and drugs through M cells. Migration pathways of mononuclear leukocytes will be traced to determine whether cells can carry antigen from the intestinal lumen into Peyer's patches. The second specific aim is to investigate modulation of Peyer's patch cytoarchitecture and function by antigenic stimulation and by depletion of regulatory lymphocyte subsets in normal mice and in a mouse model of systemic lupus erythematosus (SLE). The mechanisms by which intestinal antigen stimulation regulates surface Ig isotype switching in Peyer's patches will be evaluated by immunolabeling and fluorescence activated cell sorting (FACS). Monoclonal antibodies will be used to deplete lymphocyte subsets; the effects of subsequent changes in immunoregulatory cells on the cytoarchitecture of mucosal lymphoid organs will be assessed by immunolabeling in normal mice and in autoimmune mice in which helper T cell depletion treats SLE.