Induction by IL 1 and interferon-gamma: tissue distribution, biochemistry, and function of a natural adherence molecule (ICAM-1).
Induction by IL 1 and interferon-gamma: tissue distribution, biochemistry, and function of a natural adherence molecule (ICAM-1).
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DOI：
10.4049/jimmunol.137.1.245
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发表时间：
1986-07
影响因子：
4.4
通讯作者：
Michael Loran Dustin;R. Rothlein;A. Bhan;C. Dinarello;T. Springer
中科院分区：
文献类型：
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作者：
Michael Loran Dustin;R. Rothlein;A. Bhan;C. Dinarello;T. Springer
ICAM-1是一种细胞表面糖蛋白，最初由单克隆抗体（MAb）定义，可抑制phorbol酯刺激的白细胞聚集。冷冻切片染色和免疫荧光流式细胞术显示，细胞间粘附分子-1 （ICAM-1）表达于非造血细胞，如血管内皮细胞、胸腺上皮细胞、某些其他上皮细胞和成纤维细胞，以及造血细胞，如组织巨噬细胞、丝裂原刺激的T淋巴细胞、扁桃体、淋巴结和Peyer's斑块的生发中心树突状细胞。血管内皮细胞的ICAM-1染色在淋巴结和扁桃体的T细胞区最为强烈，表现为反应性增生。ICAM-1在外周血白细胞中少量表达。phobol酯刺激的骨髓单核细胞分化可显著增加ICAM-1的表达。白细胞介素1 （IL -1）或干扰素γ (10 U/ml)作用4或10小时后，真皮成纤维细胞上ICAM-1的表达分别增加3至5倍。这种诱导依赖于蛋白质和mRNA的合成，并且是可逆的。ICAM-1在不同的细胞类型中表现出Mr异质性，在成纤维细胞中Mr为97,000，在髓单核细胞系U937中Mr为114,000，在B淋巴母细胞样细胞JY中Mr为90,000。ICAM-1的生物合成涉及细胞内前体Mr约73,000。由tunicamycin治疗产生的非n-糖基化形式的Mr为55,000。从phorbol myristic acetate （PMA）刺激的U937中分离的ICAM-1和从成纤维细胞中分离的ICAM-1在化学脱糖基化后产生相同的Mr = 60,000的主要产物。ICAM-1 MAb干扰植物血凝素母细胞的粘附，以及SKW3细胞系与人真皮成纤维细胞层的粘附。用ICAM-1单抗预处理成纤维细胞而不是淋巴细胞，用淋巴细胞功能相关抗原1单抗预处理淋巴细胞而不是成纤维细胞，可抑制粘附。细胞间的粘附通过先前暴露于IL -1的成纤维细胞而增加，并与ICAM-1的诱导相关。
ICAM-1 is a cell surface glycoprotein originally defined by a monoclonal antibody (MAb) that inhibits phorbol ester-stimulated leukocyte aggregation. Staining of frozen sections and immunofluorescence flow cytometry showed intercellular adhesion molecule-1 (ICAM-1) is expressed on non-hematopoietic cells such as vascular endothelial cells, thymic epithelial cells, certain other epithelial cells, and fibroblasts, and on hematopoietic cells such as tissue macrophages, mitogen-stimulated T lymphocyte blasts, and germinal center dendritic cells in tonsils, lymph nodes, and Peyer's patches. ICAM-1 staining on vascular endothelial cells is most intense in T cell areas in lymph nodes and tonsils showing reactive hyperplasia. ICAM-1 is expressed in low amounts on peripheral blood leukocytes. Phorbol ester-stimulated differentiation of myelomonocytic cell lines greatly increases ICAM-1 expression. ICAM-1 expression on dermal fibroblasts is increased threefold to fivefold by either interleukin 1 (IL 1) or interferon-gamma at 10 U/ml over a period of 4 or 10 hr, respectively. The induction is dependent on protein and mRNA synthesis and is reversible. ICAM-1 displays Mr heterogeneity in different cell types with a Mr of 97,000 on fibroblasts, 114,000 on the myelomonocytic cell line U937, and 90,000 on the B lymphoblastoid cell JY. ICAM-1 biosynthesis involves a Mr approximately 73,000 intracellular precursor. The non-N-glycosylated form resulting from tunicamycin treatment has a Mr of 55,000. ICAM-1 isolated from phorbol myristic acetate (PMA) stimulated U937 and from fibroblasts yields an identical major product of Mr = 60,000 after chemical deglycosylation. ICAM-1 MAb interferes with the adhesion of phytohemagglutinin blasts, and the adhesion of the cell line SKW3 to human dermal fibroblast cell layers. Pretreatment of fibroblasts but not lymphocytes with ICAM-1 MAb, and of lymphocytes but not fibroblasts with lymphocyte function-associated antigen 1 MAb inhibits adhesion. Intercellular adhesion is increased by prior exposure of fibroblasts to IL 1, and correlates with induction of ICAM-1.