Harigai M, Hara M, Norioka K, Kitani A, Hirose T, Suzuki K, Kawakami M, Masuda K, Shinmei M, Kawagoe M
First Department of Medicine, National Defence Medical College, Tokorozawa, Japan.
Scand J Immunol. 1989 Mar;29(3):289-97. doi: 10.1111/j.1365-3083.1989.tb01127.x.
Abnormal production of immunoglobulin in the joint space is frequently observed in patients with rheumatoid arthritis (RA). We have previously demonstrated that adherent synovial cells (ASC) from patients with RA are involved in B-cell differentiation by their spontaneous production of B-cell differentiation factor (BCDF). The regulation of the production of this factor, however, has not yet been described. We investigated the effects of recombinant interleukin 1 alpha and beta (rIL-1 alpha and rIL-1 beta) on the production of BCDF in ASC. Increased production of BCDF was observed with increased rIL-1 concentration. Production of BCDF was detected 3 h after exposure of ASC to rIL-1 and increased throughout a 48-h culture. This BCDF, assayed on SKW6-CL4 cells, was found to share a common active site with interleukin 6. The effect of rIL-1 was almost neutralized by anti-IL-1 antibody and the addition of polymyxin B did not diminish the effect of rIL-1, indicating that rIL-1 itself stimulates ASC in vitro. These results suggest that IL-1 may play a regulatory role in the production of BCDF in synovial tissue.
类风湿关节炎（RA）患者关节腔内常出现免疫球蛋白的异常产生。我们之前已经证明，类风湿关节炎患者的贴壁滑膜细胞（ASC）通过自发产生B细胞分化因子（BCDF）参与B细胞分化。然而，该因子产生的调控机制尚未见报道。我们研究了重组白细胞介素1α和β（rIL-1α和rIL-1β）对ASC中BCDF产生的影响。随着rIL-1浓度的增加，BCDF的产生也增加。将ASC暴露于rIL-1 3小时后即可检测到BCDF的产生，并且在整个48小时培养过程中持续增加。在SKW6-CL4细胞上检测到的这种BCDF与白细胞介素6具有共同的活性位点。抗IL-1抗体几乎中和了rIL-1的作用，添加多粘菌素B并没有减弱rIL-1的作用，这表明rIL-1本身在体外刺激ASC。这些结果表明，IL-1可能在滑膜组织中BCDF的产生中起调节作用。
