正常及类风湿性关节炎T细胞诱导骨吸收活性

Induction of bone resorbing activity by normal and rheumatoid arthritis T cells.

作者信息

Flescher E, Garrett I R, Mundy G R, Talal N

机构信息

Division of Clinical Immunology, University of Texas Health Science Center, San Antonio.

出版信息

Clin Immunol Immunopathol. 1990 Aug;56(2):210-8. doi: 10.1016/0090-1229(90)90142-d.

DOI:10.1016/0090-1229(90)90142-d

PMID:2143127

Abstract

We studied the role of T cells in the production of osteoclast activating factor (OAF) using anti-CD3 MAb as a specific T cell activator. OAF activity was totally inhibited by anti-IL-1 beta. Peripheral blood mononuclear cells (PBMNC) from normal subjects produced more OAF than did PBMNC from rheumatoid arthritis (RA) patients. Mononuclear cells (MNC) from RA synovial fluid produced less OAF than did RA peripheral blood. We conclude that (i) specific T cell stimulation induces OAF production which may be attributed to interleukin 1 (IL-1) activity, (ii) the inhibition by anti-IL-1 beta of OAF production following anti-CD3 stimulation suggests that the T cell signal is being transmitted to the macrophage, and (iii) RA MNC are deficient in T cell-mediated OAF production.

摘要

我们使用抗CD3单克隆抗体作为特异性T细胞激活剂，研究了T细胞在破骨细胞激活因子（OAF）产生中的作用。抗IL-1β可完全抑制OAF活性。正常受试者的外周血单个核细胞（PBMNC）产生的OAF比类风湿关节炎（RA）患者的PBMNC更多。RA滑液中的单个核细胞（MNC）产生的OAF比RA外周血中的少。我们得出结论：（i）特异性T细胞刺激诱导OAF产生，这可能归因于白细胞介素1（IL-1）活性；（ii）抗IL-1β对抗CD3刺激后OAF产生的抑制表明T细胞信号正在传递给巨噬细胞；（iii）RA MNC在T细胞介导的OAF产生方面存在缺陷。