SYNOVIAL INTERLEUKIN-1 RECEPTOR ANTAGONIST AND INTERLEUKIN-1 BALANCE IN RHEUMATOID-ARTHRITIS
SYNOVIAL INTERLEUKIN-1 RECEPTOR ANTAGONIST AND INTERLEUKIN-1 BALANCE IN RHEUMATOID-ARTHRITIS
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DOI：
10.1002/art.1780370507
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发表时间：
1994-05-01
影响因子：
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通讯作者：
AREND, WP
中科院分区：
文献类型：
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作者：
FIRESTEIN, GS;BOYLE, DL;AREND, WP
Objective.目的定量类风湿关节炎（RA）滑膜组织（ST）细胞产生白细胞介素-1受体拮抗剂（IL-1 ra）和IL-1及其基因表达。通过酶联免疫吸附试验测定新鲜和培养的ST细胞、纯化的滑膜巨噬细胞和成纤维细胞样滑膜细胞（FLS）中的IL-1 α、IL-1 β和IL-1 ra蛋白水平。采用逆转录聚合酶链反应（RT-PCR）技术检测IL-1 ra的分泌型（sIL-1 ra）和选择性剪接的胞内型（icIL-1 ra）的相对表达。IL-1 α、IL-1 β和IL-1 ra存在于RA和骨关节炎患者滑膜的新鲜和培养的ST细胞样品中。IL-1 ra：IL-1比率范围为1.2至3.6，低于抑制IL-1生物活性所需的10-100倍过量IL-1 ra。分离的CD 14+滑膜巨噬细胞分泌IL-1 ra，但其量远低于肺泡或体外衍生的巨噬细胞。培养的FLS细胞内含有IL-1 ra，但很少分泌IL-1 ra到培养上清中。RT-PCR结果显示，在FLS和未分级ST细胞中，icIL-1 ra mRNA的表达量明显高于sIL-1 ra mRNA。RA ST细胞产生的IL-1 ra相对于IL-1的总产生是缺乏的。
Objective. To quantify interleukin-1 receptor antagonist (IL-1ra) and IL-1 production and gene expression by rheumatoid arthritis (RA) synovial tissue (ST) cells.Methods. IL-1 alpha, IL-1 beta, and IL-1ra protein levels were measured by enzyme-linked immunosorbent assay in fresh and cultured ST cells, purified synovial macrophages, and fibroblast-like synoviocytes (FLS). The relative expression of the secreted form of IL-1ra (sIL-1ra) and the alternatively spliced intracellular form (icIL-1ra) was determined by reverse transcription polymerase chain reaction (RT-PCR) techniques.Results. IL-1 alpha, IL-1 beta, and IL-1ra were present in fresh and cultured ST cell samples of synovium from RA and osteoarthritis patients. IL-1ra:IL-1 ratios ranged from 1.2 to 3.6, which is below the 10-100-fold excess of IL-1ra needed to inhibit IL-1 bioactivity. Isolated CD14+ synovial macrophages secreted IL-1ra, but the amount was much less than that of alveolar or in vitro-derived macrophages. Cultured FLS contained intracellular IL-1ra but secreted little IL-1ra into the culture supernatants. RT-PCR showed that icIL-1ra mRNA was more abundant than sIL-1ra mRNA in FLS and unfractionated ST cells.Conclusion. IL-1ra production by RA ST cells is deficient relative to total production of IL-1.