LFA-3, CD44, AND CD45--PHYSIOLOGIC TRIGGERS OF MONOCYTE TNF AND IL-1 RELEASE

LFA-3、CD44 和 CD45——单核细胞 TNF 和 IL-1 释放的生理触发因素

• 批准号: 3811206
• 负责人: D S WEBB
• 金额: --
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3811206
• 关键词: CD antigens; cytokine receptors; glycoproteins; human tissue; immunoregulation; leukocyte adhesion molecules; monoclonal antibody; monocyte; secretion; tumor necrosis factor alpha

The monocyte-derived cytokines, tumor necrosis factor alpha (TNF) and interleukin-1 beta (IL-1), are central regulators of the immune response, but the physiologic stimuli for their release remain largely undefined. We have found that engagement of three monocyte glycoproteins: LFA-3, CD44 and CD45 by specific monoclonal antibodies immobilized on plastic induced TNF and IL-1 release. It was shown that this response was not due to contaminating endotoxin and that five monoclonal antibodies specific for other monocyte surface antigens failed to induce TNF or IL-1 release. In addition, TNF was released when monocyte LFA-3 bound immobilized purified CD2, which is its physiologic receptor. Thus, a receptor-ligand interaction that mediates cell-cell adhesion, can transmit the necessary signals for the release of monokines.

单核细胞衍生的细胞因子，肿瘤坏死因子α（TNF）和 白细胞介素-1 β（IL-1），是免疫应答的中枢调节因子， 但其释放的生理刺激仍在很大程度上不确定。我们 已经发现三种单核细胞糖蛋白：LFA-3，CD 44和 用塑料固定的特异性单克隆抗体诱导的TNF IL-1释放结果表明，这种反应不是由于 污染的内毒素和五种特异于 其它单核细胞表面抗原不能诱导TNF或IL-1释放。在 此外，当单核细胞LFA-3结合固定化纯化时， CD 2是其生理受体。因此，受体-配体相互作用 介导细胞间粘附，可以传递必要的信号， 单核因子的释放