REGULATION OF ADHESION MOLECULE EXPRESSION ON HUMAN MONOCYTES BY CYTOKINES

单核细胞表面的黏附分子已被证明是 在IL-1和肿瘤坏死因子的触发中很重要，也被证明是 在单核细胞对肿瘤细胞的杀伤中起作用。因为他们的 在这些以及最有可能的其他单核细胞功能中的作用，我们研究了 细胞因子对单核细胞表面黏附分子表达的调节。 纯化的人单核细胞对各种细胞因子有反应 黏附蛋白表达变化的处理：Mac-1， PL50、95、ICAM-1和CD44。细胞间黏附分子-1的基础表达增强 干扰素-γ、肿瘤坏死因子、白介素4、粒-巨噬细胞集落刺激因子表达增加，而CD44表达增加。 IL-1和GM-CSF。仅GM-CSF治疗对PL50、95有影响。GM-CSF和GM-CSF IL-4促进MAC-1的表达，而干扰素和肿瘤坏死因子降低MAC-1的表达 表情。细胞因子均不能改变LFA-1和LFA-3的表达。 诱导这些蛋白表达的变化可能是一种机制 通过这些细胞因子调节单核细胞的功能，特别是 一般的免疫反应。

Adhesion molecules on the surface of monocytes have been shown to be important in the triggering of IL-1 and TNF and have also been shown to have a role in the killing of tumor cells by monocytes. Because of their role in these and most probably other monocyte functions, we studied the regulation of expression of adhesion molecules on monocytes by cytokines. Purified human monocytes were found to respond to various cytokine treatments with changes in the expression of the adhesion proteins: MAC-1, pl5O,95, ICAM-1 and CD44. Basal expression of ICAM-1 was enhanced by IFN-gamma, TNF, IL-4 and GM-CSF while CD44 expression was increased by TNF, IL-1 and GM-CSF. pl5O,95 was affected only by GM-CSF treatment. Both GM-CSF and IL-4 enhanced MAC-1 expression while IFN-gamma and TNF lowered MAC-1 expression. None of the cytokines altered LFA-1 or LFA-3 expression. Inducing changes in the expression of these proteins may be one mechanism by which cytokines regulate the functions of monocytes in particular and immune responses in general.