Berrebi Dominique, Bruscoli Stefano, Cohen Nicolas, Foussat Arnaud, Migliorati Graziella, Bouchet-Delbos Laurence, Maillot Marie-Christine, Portier Alain, Couderc Jacques, Galanaud Pierre, Peuchmaur Michel, Riccardi Carlo, Emilie Dominique
Institut National de la Santé et de la Recherche Médicale (INSERM) U131, Institut Paris-Sud sur les Cytokines, Clamart, France.
Blood. 2003 Jan 15;101(2):729-38. doi: 10.1182/blood-2002-02-0538. Epub 2002 Sep 12.
Glucocorticoids and interleukin 10 (IL-10) prevent macrophage activation. In murine lymphocytes, glucocorticoids induce expression of glucocorticoid-induced leucine zipper (GILZ), which prevents the nuclear factor kappaB (NF-kappaB)-mediated activation of transcription. We investigated whether GILZ could account for the deactivation of macrophages by glucocorticoids and IL-10. We found that GILZ was constitutively produced by macrophages in nonlymphoid tissues of humans and mice. Glucocorticoids and IL-10 stimulated the production of GILZ by macrophages both in vitro and in vivo. Transfection of the macrophagelike cell line THP-1 with the GILZ gene inhibited the expression of CD80 and CD86 and the production of the proinflammatory chemokines regulated on activation normal T-cell expressed and secreted (CCL5) and macrophage inflammatory protein 1alpha (CCL3). It also prevented toll-like receptor 2 production induced by lipopolysaccharide, interferongamma, or an anti-CD40 mAb, as well as NF-kappaB function. In THP-1 cells treated with glucocorticoids or IL-10, GILZ was associated with the p65 subunit of NF-kappaB. Activated macrophages in the granulomas of patients with Crohn disease or tuberculosis do not produce GILZ. In contrast, GILZ production persists in tumor-infiltrating macrophages in Burkitt lymphomas. Therefore, GILZ appears to play a key role in the anti-inflammatory and immunosuppressive effects of glucocorticoids and IL-10. Glucocorticoid treatment stimulates GILZ production, reproducing an effect of IL-10, a natural anti-inflammatory agent. The development of delayed-type hypersensitivity reactions is associated with the down-regulation of GILZ gene expression within lesions. In contrast, the persistence of GILZ gene expression in macrophages infiltrating Burkitt lymphomas may contribute to the failure of the immune system to reject the tumor.
糖皮质激素和白细胞介素10(IL-10)可防止巨噬细胞活化。在鼠淋巴细胞中,糖皮质激素可诱导糖皮质激素诱导亮氨酸拉链(GILZ)的表达,从而阻止核因子κB(NF-κB)介导的转录激活。我们研究了GILZ是否能解释糖皮质激素和IL-10对巨噬细胞的失活作用。我们发现,GILZ由人和小鼠非淋巴组织中的巨噬细胞组成性产生。糖皮质激素和IL-10在体外和体内均可刺激巨噬细胞产生GILZ。用GILZ基因转染巨噬细胞样细胞系THP-1可抑制CD80和CD86的表达以及促炎趋化因子正常T细胞激活后表达和分泌的趋化因子(CCL5)和巨噬细胞炎性蛋白1α(CCL3)的产生。它还可防止脂多糖、干扰素γ或抗CD40单克隆抗体诱导的Toll样受体2的产生以及NF-κB的功能。在用糖皮质激素或IL-10处理的THP-1细胞中,GILZ与NF-κB的p65亚基相关联。克罗恩病或结核病患者肉芽肿中的活化巨噬细胞不产生GILZ。相反,伯基特淋巴瘤中肿瘤浸润巨噬细胞持续产生GILZ。因此,GILZ似乎在糖皮质激素和IL-10的抗炎和免疫抑制作用中起关键作用。糖皮质激素治疗可刺激GILZ产生,重现天然抗炎剂IL-10的作用。迟发型超敏反应的发生与病变内GILZ基因表达的下调有关。相反,浸润伯基特淋巴瘤的巨噬细胞中GILZ基因表达的持续存在可能导致免疫系统无法排斥肿瘤。