• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

白细胞介素-4(IL-4)对黏附性类风湿性滑膜细胞产生白细胞介素-6(IL-6)的抑制作用。

Suppressive effect of interleukin-4 (IL-4) on IL-6 production by adherent rheumatoid synovial cells.

作者信息

Suzuki H, Sugiyama E, Tunru I S, Yamashita N, Matsuno H, Hamazaki T, Kobayashi M

机构信息

First Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.

出版信息

Clin Immunol Immunopathol. 1993 Jan;66(1):67-72. doi: 10.1006/clin.1993.1009.

DOI:10.1006/clin.1993.1009
PMID:8440075
Abstract

Interleukin-6 (IL-6) has recently been characterized as a mediator of multiple inflammatory responses. Excessive production of this cytokine has been demonstrated in the joints of patients with rheumatoid arthritis (RA). On the other hand, anti-inflammatory effects of IL-4 have recently been demonstrated. We therefore investigated the suppressive effect of IL-4 on IL-6 production by synovial cells in patients with RA. Freshly prepared adherent rheumatoid synovial cells expressed IL-6 mRNA and spontaneously produced a large amount of IL-6 in culture. This spontaneous production of IL-6 was significantly suppressed by IL-4. The suppressive effect of IL-4 on IL-6 production was demonstrated in all patients with RA tested in this study. On the other hand, IL-6 mRNA levels already expressed in adherent synovial cells were not reduced by IL-4 in 24 hr of culture. The suppressive effect of IL-4 on IL-6 production suggests that IL-4 is an important physiological regulator of IL-6 production in synovial cells.

摘要

白细胞介素-6(IL-6)最近被确定为多种炎症反应的介质。在类风湿关节炎(RA)患者的关节中已证实这种细胞因子产生过多。另一方面,最近已证实IL-4具有抗炎作用。因此,我们研究了IL-4对RA患者滑膜细胞产生IL-6的抑制作用。新鲜制备的贴壁类风湿滑膜细胞表达IL-6 mRNA,并在培养中自发产生大量IL-6。IL-4可显著抑制IL-6的这种自发产生。在本研究中测试的所有RA患者中均证实了IL-4对IL-6产生的抑制作用。另一方面,在培养24小时后,贴壁滑膜细胞中已表达的IL-6 mRNA水平并未被IL-4降低。IL-4对IL-6产生的抑制作用表明IL-4是滑膜细胞中IL-6产生的重要生理调节因子。

相似文献

1
Suppressive effect of interleukin-4 (IL-4) on IL-6 production by adherent rheumatoid synovial cells.白细胞介素-4(IL-4)对黏附性类风湿性滑膜细胞产生白细胞介素-6(IL-6)的抑制作用。
Clin Immunol Immunopathol. 1993 Jan;66(1):67-72. doi: 10.1006/clin.1993.1009.
2
Interleukin 10 cooperates with interleukin 4 to suppress inflammatory cytokine production by freshly prepared adherent rheumatoid synovial cells.白细胞介素10与白细胞介素4协同作用,抑制新鲜制备的贴壁类风湿性滑膜细胞产生炎性细胞因子。
J Rheumatol. 1995 Nov;22(11):2020-6.
3
Interleukin-4 inhibits prostaglandin E2 production by freshly prepared adherent rheumatoid synovial cells via inhibition of biosynthesis and gene expression of cyclo-oxygenase II but not of cyclo-oxygenase I.白细胞介素-4通过抑制环氧化酶II而非环氧化酶I的生物合成和基因表达,抑制新鲜制备的贴壁类风湿性滑膜细胞产生前列腺素E2。
Ann Rheum Dis. 1996 Jun;55(6):375-82. doi: 10.1136/ard.55.6.375.
4
Human interleukin-17: A T cell-derived proinflammatory cytokine produced by the rheumatoid synovium.人白细胞介素-17:一种由类风湿性滑膜产生的T细胞源性促炎细胞因子。
Arthritis Rheum. 1999 May;42(5):963-70. doi: 10.1002/1529-0131(199905)42:5<963::AID-ANR15>3.0.CO;2-E.
5
Differential in vitro effects of IL-4, IL-10, and IL-13 on proinflammatory cytokine production and fibroblast proliferation in rheumatoid synovium.白细胞介素-4、白细胞介素-10和白细胞介素-13对类风湿性滑膜炎中促炎细胞因子产生和成纤维细胞增殖的体外差异作用。
Rheumatol Int. 2001 Feb;20(2):49-54. doi: 10.1007/s002960000074.
6
An investigation of cell proliferation and soluble mediators induced by interleukin 1beta in human synovial fibroblasts: comparative response in osteoarthritis and rheumatoid arthritis.白细胞介素1β诱导人滑膜成纤维细胞的细胞增殖及可溶性介质的研究:骨关节炎与类风湿关节炎的比较反应
Inflamm Res. 2001 Feb;50(2):65-72. doi: 10.1007/s000110050726.
7
Interleukin-4 inhibits interleukin-11 production by rheumatoid synovial cells.白细胞介素-4抑制类风湿性滑膜细胞产生白细胞介素-11。
Rheumatology (Oxford). 2000 Jul;39(7):728-31. doi: 10.1093/rheumatology/39.7.728.
8
FK506, an immunosuppressant, partially inhibits interleukin 6 production by adherent rheumatoid synovial cells.免疫抑制剂FK506可部分抑制黏附性类风湿性滑膜细胞产生白细胞介素6。
J Rheumatol. 1994 Sep;21(9):1597-601.
9
Expression of interleukin-12 in synovial tissue from patients with rheumatoid arthritis.类风湿关节炎患者滑膜组织中白细胞介素-12的表达。
Arthritis Rheum. 1998 Feb;41(2):306-14. doi: 10.1002/1529-0131(199802)41:2<306::AID-ART15>3.0.CO;2-4.
10
Protein tyrosine phosphatase nonreceptor type 2: an important regulator of lnterleukin-6 production in rheumatoid arthritis synovial fibroblasts.蛋白酪氨酸磷酸酶非受体型 2:类风湿关节炎滑膜成纤维细胞中白细胞介素-6 产生的重要调节因子。
Arthritis Rheumatol. 2015 Oct;67(10):2624-33. doi: 10.1002/art.39256.

引用本文的文献

1
Significance of Interleukin (IL)-4 and IL-13 in Inflammatory Arthritis.白细胞介素 (IL)-4 和 IL-13 在炎症性关节炎中的意义。
Cells. 2021 Nov 3;10(11):3000. doi: 10.3390/cells10113000.
2
Effect of interleukin-4 on vascular endothelial growth factor production in rheumatoid synovial fibroblasts.白细胞介素-4对类风湿性滑膜成纤维细胞中血管内皮生长因子产生的影响。
Clin Exp Immunol. 2007 Mar;147(3):573-9. doi: 10.1111/j.1365-2249.2006.03295.x.
3
Gene therapy for established murine collagen-induced arthritis by local and systemic adenovirus-mediated delivery of interleukin-4.
通过局部和全身腺病毒介导的白细胞介素-4递送对已建立的小鼠胶原诱导性关节炎进行基因治疗。
Arthritis Res. 2000;2(4):293-302. doi: 10.1186/ar104. Epub 2000 May 24.
4
IL-17 regulates gene expression and protein synthesis of the complement system, C3 and factor B, in skin fibroblasts.白细胞介素-17调节皮肤成纤维细胞中补体系统、C3和B因子的基因表达及蛋白质合成。
Clin Exp Immunol. 2000 Apr;120(1):22-9. doi: 10.1046/j.1365-2249.2000.01199.x.
5
Cytokines affecting megakaryocytopoiesis in rheumatoid arthritis with thrombocytosis.类风湿关节炎血小板增多症中影响巨核细胞生成的细胞因子
Rheumatol Int. 1996;16(1):5-8. doi: 10.1007/BF01419947.
6
Interleukin-4 inhibits prostaglandin E2 production by freshly prepared adherent rheumatoid synovial cells via inhibition of biosynthesis and gene expression of cyclo-oxygenase II but not of cyclo-oxygenase I.白细胞介素-4通过抑制环氧化酶II而非环氧化酶I的生物合成和基因表达,抑制新鲜制备的贴壁类风湿性滑膜细胞产生前列腺素E2。
Ann Rheum Dis. 1996 Jun;55(6):375-82. doi: 10.1136/ard.55.6.375.