Enhanced production of interleukin-6 in mice with type II collagen-induced arthritis.
Enhanced production of interleukin-6 in mice with type II collagen-induced arthritis.
复制标题
增强 II 型胶原诱导关节炎小鼠体内白细胞介素 6 的产生。
作者：
Y. Takai;N. Seki;H. Senoh;T. Yokota;F. Lee;T. Hamaoka;H. Fujiwara
我们从小鼠浆细胞瘤MOPC-104 E细胞中建立了白细胞介素-6（IL-6）依赖性细胞系。发现该细胞系（命名为PIL-6）对鼠和人IL-6有反应，但对任何其他细胞因子没有反应。我们使用该细胞系研究DBA/1小鼠II型胶原诱导的关节炎中IL-6产生的参与。仅在DBA/1小鼠的血清中检测到边际IL-6活性，所述DBA/1小鼠单独接种弗氏完全佐剂（FCA）、接种不相关蛋白（牛血清白蛋白）加FCA或接种II型胶原加弗氏不完全佐剂。然而，在注射II型胶原和FCA诱导关节炎的DBA/1小鼠中观察到IL-6活性增强。血清IL-6活性水平的升高与关节炎小鼠淋巴结细胞在体外用II型胶原刺激时产生的高水平IL-6相关。我们还发现，L3 T4 + T细胞亚群负责关节炎小鼠中IL-6的产生增强。结果进行了讨论的背景下，IL-6的诱导和/或表达的慢性，进行性关节炎的潜在作用。
We established an interleukin-6 (IL-6)-dependent cell line from murine plasmacytoma MOPC-104E cells. This cell line (designated PIL-6) was found to respond to murine and to human IL-6, but not to any other cytokines. We used this cell line to investigate the involvement of IL-6 production in type II collagen-induced arthritis in DBA/1 mice. Only marginal IL-6 activity was detected in sera from DBA/1 mice inoculated with Freund's complete adjuvant (FCA) alone, with an unrelated protein (bovine serum albumin) plus FCA, or with type II collagen plus Freund's incomplete adjuvant. However, enhanced IL-6 activity was observed in DBA/1 mice that had been injected with type II collagen plus FCA to induce arthritis. The elevated level of serum IL-6 activity was associated with high levels of IL-6 produced when lymph node cells from arthritic mice were stimulated in vitro with type II collagen. We also found that the L3T4+ T cell subset is responsible for the enhanced production of IL-6 in arthritic mice. The results are discussed in the context of potential roles of IL-6 in the induction and/or expression of chronic, progressive arthritis.
来自患有胶原诱导关节炎的小鼠的 II 型胶原反应性 T 细胞克隆。
DOI：
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发表时间：
1985
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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作者：
Dallman,M;Fathman,CG
通讯作者：
Fathman,CG
佐剂性关节炎中致关节炎因子的检测。
DOI：
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发表时间：
1988
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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作者：
Helfgott,SM;Kieval,RI;Breedveld,FC;Brahn,E;Young,CT;Dynesius-Trentham,R;Trentham,DE
通讯作者：
Trentham,DE