Temime N, Joliviere A, Lando D, Teyton L, Charron D
Laboratoire d'Immunogénétique Moléculaire, Institut Biomédical des Cordeliers, Paris, France.
Hum Immunol. 1991 Aug;31(4):261-70. doi: 10.1016/0198-8859(91)90098-t.
Interleukin 1 (IL-1) exerts biological properties on various immune and nonimmune cell types and tissues and thus may play an important role during chronic inflammatory processes. Here we have examined the IL-1 biosynthesis in adherent synovial lining cell (ASLC) cultures obtained from patients with rheumatoid arthritis (RA). We report that ASLCs in culture showed heterogeneous endogenous levels of IL-1 alpha and beta expression. Recombinant interleukin 1 (rIL-1) alpha or beta induced increases of IL-1 alpha and beta mRNA and proteins levels in ASLCs. Although IL-1 synthesis is enhanced by rIL-1 treatment, no soluble IL-1 alpha or beta could be detected by specific enzyme-linked immunosorbent assays. A pretreatment with recombinant IFN gamma (rIFN gamma) down-regulated the effect of rIL-1 on IL-1 synthesis in ASLCs. Actinomycin D suppressed the endogeneous and rIL-1-induced IL-1 mRNA expression Indomethacin, in the presence of rIL-1 alpha or beta, up-regulates the level of expression of IL-1 beta in ASLCs pretreated with rIFN gamma, but has the opposite effect in non-pretreated cells. The increase of IL-1 gene expression by rIL-1 in human ASLCs from RA patients may contribute as an amplification of the disease progress. These studies may also explain the beneficial effects of IFN gamma in experimental models of IL-1-induced bone and cartilage degradation and in patients with diseases involving IL-1.
白细胞介素1（IL-1）对多种免疫和非免疫细胞类型及组织发挥生物学作用，因此可能在慢性炎症过程中起重要作用。在此，我们检测了从类风湿关节炎（RA）患者获取的贴壁滑膜衬里细胞（ASLC）培养物中的IL-1生物合成。我们报告，培养中的ASLC显示出IL-1α和β表达的内源性水平存在异质性。重组白细胞介素1（rIL-1）α或β诱导ASLC中IL-1α和β mRNA及蛋白质水平升高。尽管rIL-1处理可增强IL-1合成，但通过特异性酶联免疫吸附测定法未检测到可溶性IL-1α或β。用重组干扰素γ（rIFNγ）预处理可下调rIL-1对ASLC中IL-1合成的作用。放线菌素D抑制内源性和rIL-1诱导的IL-1 mRNA表达。在存在rIL-1α或β的情况下，吲哚美辛上调了用rIFNγ预处理的ASLC中IL-1β的表达水平，但在未预处理的细胞中具有相反的作用。rIL-1在RA患者的人ASLC中增加IL-1基因表达可能有助于疾病进展的放大。这些研究也可能解释了IFNγ在IL-1诱导的骨和软骨降解实验模型以及涉及IL-1的疾病患者中的有益作用。
