• 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增强小鼠细胞毒性T细胞依赖白细胞介素-2的增殖。

IL-4 potentiates the IL-2-dependent proliferation of mouse cytotoxic T cells.

作者信息

Miller C L, Hooton J W, Gillis S, Paetkau V

机构信息

Department of Biochemistry, University of Alberta, Edmonton, Canada.

出版信息

J Immunol. 1990 Feb 15;144(4):1331-7.

PMID:2137490
Abstract

In addition to the regulation of B lymphocyte growth and differentiation, the cytokine IL-4 (BSF-1) exerts effects on T lymphocytes and other bone marrow-derived lineages. We show here that recombinant mouse IL-4 synergizes with low levels of IL-2 to increase the yield of cytotoxic activity in a primary MLR, and the proliferation of both cloned IL-2-dependent CTL lines and cells obtained from a primary MLR. IL-4 did not induce the proliferation of any of several cloned CTL cell lines on its own. It also did not replace IL-2 in stimulating the growth or reactivation of quiescent, antigen-dependent CTL clones. However, IL-4 was synergistic with IL-2 after reactivation of the quiescent cells with antigen plus IL-2. Enhancement by IL-4 of the IL-2-driven proliferation of an antigen-independent line was blocked by the addition of anti-IL-4 monoclonal antibody. Although incubation of the CTL clones with IL-4 or with IL-2 plus IL-4 induced a transient increase in the expression of the mRNA encoding the 55 kDa IL-2 receptor, no change in the number or affinity of IL-2 receptors because of IL-4 was detected. This suggests that IL-4 does not potentiate the IL-2 response by altering IL-2 receptor levels. Instead, we propose that the synergistic effect of IL-4 is mediated by a different signalling mechanism from that used by IL-2.

摘要

除了调节B淋巴细胞的生长和分化外,细胞因子白细胞介素-4(BSF-1)还对T淋巴细胞和其他骨髓来源的细胞谱系产生作用。我们在此表明,重组小鼠白细胞介素-4与低水平的白细胞介素-2协同作用,可提高初次混合淋巴细胞反应(MLR)中细胞毒性活性的产量,以及克隆的白细胞介素-2依赖性细胞毒性T淋巴细胞(CTL)系和从初次MLR获得的细胞的增殖。白细胞介素-4自身不会诱导几种克隆的CTL细胞系中的任何一种增殖。在刺激静止的、抗原依赖性CTL克隆的生长或再激活方面,它也不能替代白细胞介素-2。然而,在用抗原加白细胞介素-2使静止细胞再激活后,白细胞介素-4与白细胞介素-2具有协同作用。添加抗白细胞介素-4单克隆抗体可阻断白细胞介素-4对白细胞介素-2驱动的非抗原依赖性细胞系增殖的增强作用。尽管用白细胞介素-4或白细胞介素-2加白细胞介素-4孵育CTL克隆会导致编码55 kDa白细胞介素-2受体的mRNA表达短暂增加,但未检测到由于白细胞介素-4导致的白细胞介素-2受体数量或亲和力的变化。这表明白细胞介素-4不会通过改变白细胞介素-2受体水平来增强白细胞介素-2反应。相反,我们提出白细胞介素-4的协同作用是由一种与白细胞介素-2不同的信号传导机制介导的。

相似文献

1
IL-4 potentiates the IL-2-dependent proliferation of mouse cytotoxic T cells.白细胞介素-4增强小鼠细胞毒性T细胞依赖白细胞介素-2的增殖。
J Immunol. 1990 Feb 15;144(4):1331-7.
2
Development of precytotoxic T cells in cyclosporine-suppressed mixed lymphocyte reactions.环孢素抑制的混合淋巴细胞反应中细胞毒性前体T细胞的发育
J Immunol. 1990 Feb 1;144(3):816-23.
3
IL-2-dependent proliferation of murine T cells requires expression of both the p55 and p70 subunits of the IL-2 receptor.小鼠T细胞依赖白细胞介素-2(IL-2)的增殖需要IL-2受体的p55和p70亚基都表达。
J Immunol. 1990 Dec 15;145(12):4136-44.
4
Tumor promoters in conjunction with calcium ionophores mimic antigenic stimulation by reactivation of alloantigen-primed murine T lymphocytes.肿瘤启动子与钙离子载体共同作用,通过重新激活同种抗原致敏的小鼠T淋巴细胞来模拟抗原刺激。
J Immunol. 1985 Dec;135(6):3674-80.
5
Cyclosporine blocks the activation of antigen-dependent cytotoxic T lymphocytes directly by an IL-2-independent mechanism.环孢素通过一种不依赖白细胞介素-2的机制直接阻断抗原依赖性细胞毒性T淋巴细胞的激活。
J Immunol. 1988 May 15;140(10):3303-8.
6
Autocrine growth of T cells independent of interleukin 2: identification of interleukin 4 (IL 4, BSF-1) as an autocrine growth factor for a cloned antigen-specific helper T cell.不依赖白细胞介素2的T细胞自分泌生长:鉴定白细胞介素4(IL-4,BSF-1)为克隆的抗原特异性辅助性T细胞的自分泌生长因子。
J Immunol. 1987 Jun 15;138(12):4280-7.
7
Antigen-independent activation of memory cytotoxic T cells by interleukin 2.白细胞介素2对记忆性细胞毒性T细胞的抗原非依赖性激活。
J Immunol. 1984 Apr;132(4):1845-50.
8
Regulatory effects of transforming growth factor-beta on IL-2- and IL-4-dependent T cell-cycle progression.转化生长因子-β对白细胞介素-2和白细胞介素-4依赖的T细胞周期进程的调节作用。
J Immunol. 1990 Mar 1;144(5):1767-76.
9
Regulation of interleukin 2 receptor expression on murine cytotoxic T lymphocyte clones.小鼠细胞毒性T淋巴细胞克隆上白细胞介素2受体表达的调控
J Immunol. 1984 Feb;132(2):839-44.
10
Effects of IL-12 on the generation of cytotoxic activity in human CD8+ T lymphocytes.白细胞介素-12对人CD8 + T淋巴细胞细胞毒性活性产生的影响。
J Immunol. 1993 Sep 1;151(5):2444-52.

引用本文的文献

1
Demystifying the cytokine network: Mathematical models point the way.揭开细胞因子网络的神秘面纱:数学模型指明方向。
Cytokine. 2017 Oct;98:115-123. doi: 10.1016/j.cyto.2016.11.013. Epub 2016 Dec 3.
2
Systemic reduction of interleukin-4 or interleukin-10 fails to reduce the frequency or severity of experimental cytomegalovirus retinitis in mice with retrovirus-induced immunosuppression.在逆转录病毒诱导免疫抑制的小鼠中,全身性降低白细胞介素-4或白细胞介素-10并不能降低实验性巨细胞病毒性视网膜炎的发生率或严重程度。
Ophthalmol Eye Dis. 2012 Sep 25;4:79-90. doi: 10.4137/OED.S10294. Print 2012.
3
Interleukin-4 impairs granzyme-mediated cytotoxicity of Simian virus 40 large tumor antigen-specific CTL in BALB/c mice.
白细胞介素-4损害BALB/c小鼠中猿猴病毒40大肿瘤抗原特异性细胞毒性T淋巴细胞的颗粒酶介导的细胞毒性。
Cancer Immunol Immunother. 2007 Oct;56(10):1625-36. doi: 10.1007/s00262-007-0309-0. Epub 2007 Apr 13.
4
Th1/Th2 balance in cancer, transplantation and pregnancy.癌症、移植及妊娠中的Th1/Th2平衡
Springer Semin Immunopathol. 1999;21(3):339-59. doi: 10.1007/BF00812261.
5
Modification of the Sendai virus-specific antibody and CD8+ T-cell responses in mice homozygous for disruption of the interleukin-4 gene.白细胞介素-4基因敲除纯合小鼠中仙台病毒特异性抗体和CD8 + T细胞反应的改变
J Virol. 1997 Mar;71(3):2518-21. doi: 10.1128/JVI.71.3.2518-2521.1997.
6
Making sense of the combined effect of interleukin-2 and interleukin-4 on lymphocytes using a mathematical model.使用数学模型理解白细胞介素-2和白细胞介素-4对淋巴细胞的联合作用。
Bull Math Biol. 1996 May;58(3):569-94. doi: 10.1007/BF02460597.
7
Activity of CD4+ T-cell clones of type 1 and type 2 in generation of influenza virus-specific cytotoxic responses in vitro.1型和2型CD4 + T细胞克隆在体外产生流感病毒特异性细胞毒性反应中的活性。
J Virol. 1991 Nov;65(11):6071-6. doi: 10.1128/JVI.65.11.6071-6076.1991.