PERIPHERAL-BLOOD AND SYNOVIAL-FLUID MONOCYTE ACTIVATION IN INFLAMMATORY ARTHRITIS .2. LOW-LEVELS OF SYNOVIAL-FLUID AND SYNOVIAL TISSUE INTERFERON SUGGEST THAT GAMMA-INTERFERON IS NOT THE PRIMARY MACROPHAGE ACTIVATING FACTOR
PERIPHERAL-BLOOD AND SYNOVIAL-FLUID MONOCYTE ACTIVATION IN INFLAMMATORY ARTHRITIS .2. LOW-LEVELS OF SYNOVIAL-FLUID AND SYNOVIAL TISSUE INTERFERON SUGGEST THAT GAMMA-INTERFERON IS NOT THE PRIMARY MACROPHAGE ACTIVATING FACTOR
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DOI：
10.1002/art.1780300804
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发表时间：
1987-08-01
影响因子：
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通讯作者：
ZVAIFLER, NJ
中科院分区：
文献类型：
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作者：
FIRESTEIN, GS;ZVAIFLER, NJ
因为炎性关节炎患者的滑液单核细胞（SFM）具有活化的表型（即，HLA-DR的高表达和单核细胞分化抗原Mo 2的低表达），我们评估了γ-干扰素（γ- IFN）在这些细胞的活化中。灵敏和特异的放射免疫测定仅检测到0.40 ±。0.20单位/ml的γ-类风湿性关节炎（RA）患者SF中的IFN和0.61 ± 0.01。0.67单位/ml的γ-其他形式慢性炎症性关节炎患者SF中的IFN。没有检测到α-通过放射免疫测定法研究任何SF中的IFN。生物测定未能检测到非免疫反应性IFN。滑膜组织（ST）外植体产生非常少的γ- IFN（0.04 ± 0.001）; 0.091单位/ml），并且在培养物中存在吲哚美辛或去除贴壁细胞并不增加产量。然而，γ-如果ST在植物血凝素的存在下培养，则产生IFN。在SF和ST上清液中，γ- IFN介导的单核细胞HLA-DR诱导被抑制，即使免疫反应性IFN的量不受影响。前列腺素E2被证明是一种可能的抑制剂。我们证明了在某些个体的外周血单核细胞上诱导HLA-DR的因子，并且不能被单克隆抗-γ-DR中和。IFN抗体存在于SF和ST上清液中。这些数据表明，SFM的激活可能通过γ以外的机制发生。的IFN
Because synovial fluid monocytes (SFM) in patients with inflammatory arthritis bear an activated phenotype (i.e., high expression of HLA-DR and low expression of the monocyte differentiation antigen Mo2), we assessed the role of .gamma.-interferon (.gamma.-IFN) in the activation of these cells. Sensitive and specific radioimmunoassays detected only 0.40 .+-. 0.20 units/ml of .gamma.-IFN in the SF of patients with rheumatoid arthritis (RA) and 0.61 .+-. 0.67 units/ml of .gamma.-IFN in the SF of patients with other forms of chronic inflammatory arthritis. There was no detectable .alpha.-IFN in any SF studied by radioimmunoassay. Bioassays failed to detect nonimmunoreactive IFN. Synovial tissue (ST) explants produced very little .gamma.-IFN (0.04 .+-. 0.091 units/ml), and production was not increased by the presence of indomethacin in the cultures or by removal of adherent cells. However, .gamma.-IFN was produced if ST was cultivated in the presence of phytohemagglutinin. In SF and ST supernatants, .gamma.-IFN-mediated induction of HLA-DR on monocytes was inhibited, even though the amount of immunoreactive IFN was not affected. Prostaglandin E2 was shown to be one possible inhibitor. We demonstrated that a factor that induces HLA-DR on some individual''s peripheral blood monocytes, and cannot be neutralized by monoclonal anti-.gamma.-IFN antibody, is present in SF and ST supernatants. These data suggest that activation of SFM may occur by mechanisms other than .gamma.-IFN.