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本文引用的文献

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Phenotypic characterization of synovial tissue cells in situ in different types of synovitis.不同类型滑膜炎中滑膜组织细胞的原位表型特征
Arthritis Rheum. 1983 Nov;26(11):1321-32. doi: 10.1002/art.1780261104.
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Collagen-induced arthritis in rats: antigen-specific suppression of arthritis and immunity by intravenously injected native type II collagen.大鼠胶原诱导性关节炎：静脉注射天然II型胶原对关节炎和免疫的抗原特异性抑制
J Immunol. 1983 Dec;131(6):2995-3000.
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Capacity of mycobacterial wax D and its subfractions to induce adjuvant arthritis in rats.分枝杆菌蜡质D及其亚组分诱导大鼠佐剂性关节炎的能力。
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The ability of bacterial lipopolysaccharide to modulate the induction of unresponsiveness to a state of immunity. Cellular parameters.细菌脂多糖将无反应性诱导调节至免疫状态的能力。细胞参数。
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Prevention of type II collagen-induced arthritis by in vivo treatment with anti-L3T4.通过体内抗L3T4治疗预防II型胶原诱导的关节炎。
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Cloning and expression in Escherichia coli of the cDNA for murine tumor necrosis factor.小鼠肿瘤坏死因子cDNA在大肠杆菌中的克隆与表达
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Identification of immunostimulatory dendritic cells in the synovial effusions of patients with rheumatoid arthritis.类风湿关节炎患者滑膜积液中免疫刺激性树突状细胞的鉴定。
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Effects of cyclosporin on collagen induced arthritis in mice.环孢素对小鼠胶原诱导性关节炎的影响。
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内源性肿瘤坏死因子α和转化生长因子β在小鼠II型胶原性关节炎诱导过程中的作用。

Involvement of endogenous tumor necrosis factor alpha and transforming growth factor beta during induction of collagen type II arthritis in mice.

作者信息

Thorbecke G J, Shah R, Leu C H, Kuruvilla A P, Hardison A M, Palladino M A

机构信息

Department of Pathology, New York University School of Medicine, NY 10016.

出版信息

Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7375-9. doi: 10.1073/pnas.89.16.7375.

DOI:10.1073/pnas.89.16.7375
PMID:1502148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC49712/
Abstract

Both tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta) are found in synovial fluid from arthritic joints of humans and of rodents with experimental arthritis. The role of endogenously produced TGF-beta and TNF in the pathogenesis of collagen type II-induced arthritis (CIA) in DBA/1 mice was examined by determining the effect of neutralizing monoclonal antibodies to these factors on the course of the disease. Endogenously produced as well as systemically administered TGF-beta 1 and TNF-alpha had opposite effects, since TGF-beta 1 and anti-TNF protected against CIA, whereas anti-TGF-beta and TNF-alpha increased CIA incidence and/or severity. Intraperitoneally injected TGF-beta 1 at a dose of 2 micrograms per day for 14 days significantly ameliorated arthritis, even when started at the time of arthritis development, although it did not reverse established disease. The resistance to CIA induction caused by a prior intravenous injection of collagen type II was not significantly influenced by the simultaneous injection of TGF-beta 1, TNF-alpha, or interleukin 1 alpha. It is concluded that the endogenous production of TNF and TGF-beta is important in determining the course of CIA.

摘要

肿瘤坏死因子α（TNF-α）和转化生长因子β（TGF-β）在人类关节炎关节以及实验性关节炎啮齿动物的滑液中均有发现。通过测定针对这些因子的中和单克隆抗体对疾病进程的影响，研究了内源性产生的TGF-β和TNF在DBA/1小鼠II型胶原诱导性关节炎（CIA）发病机制中的作用。内源性产生的以及全身给药的TGF-β1和TNF-α具有相反的作用，因为TGF-β1和抗TNF可预防CIA，而抗TGF-β和TNF-α则增加CIA的发病率和/或严重程度。每天腹腔注射2微克TGF-β1，持续14天，即使在关节炎发病时开始注射，也能显著改善关节炎，尽管它不能逆转已有的疾病。预先静脉注射II型胶原对CIA诱导的抗性，不会因同时注射TGF-β1、TNF-α或白细胞介素1α而受到显著影响。得出的结论是，TNF和TGF-β的内源性产生在决定CIA的进程中很重要。