• 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

单核细胞在微生物有丝分裂原诱导的小鼠B和T淋巴细胞早期激活标志物CD69上调中的作用。

Role of monocytes in the up-regulation of the early activation marker CD69 on B and T murine lymphocytes induced by microbial mitogens.

作者信息

Vilanova M, Tavares D, Ferreira P, Oliveira L, Nóbrega A, Appelberg R, Arala-Chaves M

机构信息

Department of Immunology, Institute for Biomedical Sciences Abel Salazar, Porto, Portugal.

出版信息

Scand J Immunol. 1996 Feb;43(2):155-63. doi: 10.1046/j.1365-3083.1996.d01-25.x.

DOI:10.1046/j.1365-3083.1996.d01-25.x
PMID:8633195
Abstract

CD69 is an early marker of lymphoid cell activation. The authors report on an up-regulation of CD69 in splenic B and T cells of C57Bl/6 mice after administration of lipopolysaccharide (LPS) or microbial immunosuppressive/mitogenic (ISM) proteins produced by C. albicans (p43) and African Swine Fever Virus (p36). This up-regulation of CD69 was observed 6 and 24 h after mitogenic treatments. The same pattern of increased CD69 expression was observed in the lymph nodes of mice treated with p43 or LPS, whereas p36 treatment failed to induce increased CD69 expression in this organ. Intracellular calcium mobilization was induced in splenic B and T lymphocytes after incubation of total spleen cells with LPS, p43 or p36. This increase was higher in B than in T cells. Increased calcium mobilization was also seen in lymph node B cells after incubation with p43 or p36 and in lymph node T cells after p43 stimulation. Up-regulation of CD69 expression on B and T cells was also observed after in vitro stimulation of spleen cells with the three mitogens used. Similar results were obtained with culture supernatants of macrophage/monocyte (M phi) cells activated with LPS (LPS/M phi CS). Stimulation of M phi cells with LPS or with the ISM proteins is demonstrated by the increased production of nitrites by these cells. The increased in vitro expression of CD69 was, however, not abolished by monoclonal antibodies to M phi cytokines such as IL-6, IL-10 or TNF alpha. No increased expression of CD69 was found in vitro on purified B or T cells, even when mixed upon stimulation with p43, p36, LPS or with LPS/M phi CS. However, an increase in the expression of CD69 was observed on B cells co-cultured with M phi cells after treatment with LPS or p36. All three mitogens failed to induce increased CD69 expression on cultured T cells mixed with M phi cells.

摘要

CD69是淋巴细胞活化的早期标志物。作者报告称,在给C57Bl/6小鼠注射脂多糖(LPS)或白色念珠菌(p43)和非洲猪瘟病毒(p36)产生的微生物免疫抑制/促有丝分裂(ISM)蛋白后,其脾脏B细胞和T细胞中CD69上调。在促有丝分裂处理后6小时和24小时观察到这种CD69上调。在用p43或LPS处理的小鼠淋巴结中观察到相同的CD69表达增加模式,而p36处理未能诱导该器官中CD69表达增加。在用LPS、p43或p36孵育全脾细胞后,脾脏B淋巴细胞和T淋巴细胞中诱导了细胞内钙动员。这种增加在B细胞中比在T细胞中更高。在用p43或p36孵育后,淋巴结B细胞中也观察到钙动员增加,在p43刺激后,淋巴结T细胞中也观察到钙动员增加。在用三种促有丝分裂原体外刺激脾细胞后,也观察到B细胞和T细胞上CD69表达上调。用LPS激活的巨噬细胞/单核细胞(M phi)细胞的培养上清液(LPS/M phi CS)也获得了类似结果。用LPS或ISM蛋白刺激M phi细胞可通过这些细胞中亚硝酸盐产量增加来证明。然而,针对M phi细胞因子如IL-6、IL-10或TNFα的单克隆抗体并未消除体外CD69表达的增加。在纯化的B细胞或T细胞上,即使在用p43、p36、LPS或LPS/M phi CS刺激时混合,也未发现体外CD69表达增加。然而,在用LPS或p36处理后,与M phi细胞共培养的B细胞上观察到CD69表达增加。所有三种促有丝分裂原均未能在与M phi细胞混合培养的T细胞上诱导CD69表达增加。

相似文献

1
Role of monocytes in the up-regulation of the early activation marker CD69 on B and T murine lymphocytes induced by microbial mitogens.单核细胞在微生物有丝分裂原诱导的小鼠B和T淋巴细胞早期激活标志物CD69上调中的作用。
Scand J Immunol. 1996 Feb;43(2):155-63. doi: 10.1046/j.1365-3083.1996.d01-25.x.
2
Platelets inhibit in vitro response of lymphocytes to mitogens.血小板可抑制淋巴细胞在体外对有丝分裂原的反应。
Immunol Lett. 2008 Aug 15;119(1-2):57-61. doi: 10.1016/j.imlet.2008.04.003. Epub 2008 May 14.
3
LPS regulation of the immune response: separate mechanisms for murine B cell activation by lipid A (direct) and polysaccharide (macrophage-dependent) derived from Bacteroides LPS.脂多糖对免疫反应的调节:来自拟杆菌属脂多糖的脂质A(直接作用)和多糖(巨噬细胞依赖性)激活小鼠B细胞的不同机制。
J Immunol. 1984 Nov;133(5):2294-300.
4
Abnormalities in CD69 expression, cytosolic pH and Ca2+ during activation of lymphocytes from patients with systemic lupus erythematosus.系统性红斑狼疮患者淋巴细胞激活过程中CD69表达、胞质pH值和Ca2+的异常情况。
Lupus. 1997;6(1):48-56. doi: 10.1177/096120339700600107.
5
Ixodes ricinus tick salivary gland extract inhibits IL-10 secretion and CD69 expression by mitogen-stimulated murine splenocytes and induces hyporesponsiveness in B lymphocytes.蓖麻硬蜱唾液腺提取物可抑制丝裂原刺激的小鼠脾细胞分泌白细胞介素-10及表达CD69,并诱导B淋巴细胞反应低下。
Parasite Immunol. 2003 Jan;25(1):27-37. doi: 10.1046/j.1365-3024.2003.00605.x.
6
Improved four-color flow cytometry method using fluo-3 and triple immunofluorescence for analysis of intracellular calcium ion ([Ca2+]i) fluxes among mouse lymph node B- and T-lymphocyte subsets.使用Fluo-3和三重免疫荧光的改进型四色流式细胞术方法,用于分析小鼠淋巴结B淋巴细胞和T淋巴细胞亚群中的细胞内钙离子([Ca2+]i)通量。
Cytometry. 1996 Mar 1;23(3):205-17. doi: 10.1002/(SICI)1097-0320(19960301)23:3<205::AID-CYTO4>3.0.CO;2-H.
7
Donor cell induced CD69 expression and intracellular IL-2 and IL-4 production by peripheral blood lymphocytes isolated from kidney transplant recipients.供体细胞诱导肾移植受者外周血淋巴细胞表达CD69并产生细胞内白细胞介素-2和白细胞介素-4 。
Hum Immunol. 1999 Jan;60(1):41-56. doi: 10.1016/s0198-8859(98)00091-3.
8
Induction of surface antigen CD69 expression in T-lymphocytes following exposure to actinomycin D.放线菌素D处理后T淋巴细胞表面抗原CD69表达的诱导。
Int J Immunopharmacol. 1999 Oct;21(10):689-703. doi: 10.1016/s0192-0561(99)00045-4.
9
The biological effects induced in mice by p36, a proteinaceous factor of virulence produced by African swine fever virus, are mediated by interleukin-4 and also to a lesser extent by interleukin-10.由非洲猪瘟病毒产生的一种毒性蛋白因子p36在小鼠体内诱导产生的生物学效应,是由白细胞介素-4介导的,并且在较小程度上也由白细胞介素-10介导。
Immunology. 1999 Mar;96(3):389-95. doi: 10.1046/j.1365-2567.1999.00629.x.
10
The effect of glutamine on murine splenic leukocyte responses to T and B cell mitogens.谷氨酰胺对小鼠脾脏白细胞对T细胞和B细胞有丝分裂原反应的影响。
Immunol Cell Biol. 1990 Dec;68 ( Pt 6):405-8. doi: 10.1038/icb.1990.54.

引用本文的文献

1
Mild Cognitive Impairment Is Associated with Enhanced Activation of Th17 Lymphocytes in Non-Alcoholic Fatty Liver Disease.轻度认知障碍与非酒精性脂肪性肝病中 Th17 淋巴细胞的过度激活有关。
Int J Mol Sci. 2023 Jun 20;24(12):10407. doi: 10.3390/ijms241210407.
2
Minimal hepatic encephalopathy is associated with expansion and activation of CDCD28, Th22 and Tfh and B lymphocytes.轻微型肝性脑病与 CDCD28、Th22 和 Tfh 及 B 淋巴细胞的扩增和激活有关。
Sci Rep. 2017 Jul 27;7(1):6683. doi: 10.1038/s41598-017-05938-1.
3
Full activation of CD4+ T cells early during sepsis requires specific antigen.
脓毒症早期CD4+ T细胞的完全激活需要特定抗原。
Shock. 2015 Feb;43(2):192-200. doi: 10.1097/SHK.0000000000000267.
4
The presence of CD8+ invariant NKT cells in mice.在小鼠中存在 CD8+ 不变自然杀伤 T 细胞。
Exp Mol Med. 2009 Dec 31;41(12):866-72. doi: 10.3858/emm.2009.41.12.092.
5
Neisserial outer membrane vesicles bind the coinhibitory receptor carcinoembryonic antigen-related cellular adhesion molecule 1 and suppress CD4+ T lymphocyte function.奈瑟菌外膜囊泡结合共抑制受体癌胚抗原相关细胞黏附分子1并抑制CD4+ T淋巴细胞功能。
Infect Immun. 2007 Sep;75(9):4449-55. doi: 10.1128/IAI.00222-07. Epub 2007 Jul 9.
6
Human immunodeficiency virus-like particles activate multiple types of immune cells.人类免疫缺陷病毒样颗粒可激活多种类型的免疫细胞。
Virology. 2007 Jun 5;362(2):331-41. doi: 10.1016/j.virol.2006.12.014. Epub 2007 Feb 5.
7
Characterization of the B-cell immune response elicited in BALB/c mice challenged with Neospora caninum tachyzoites.用犬新孢子虫速殖子攻击BALB/c小鼠后引发的B细胞免疫反应的特征
Immunology. 2005 Sep;116(1):38-52. doi: 10.1111/j.1365-2567.2005.02195.x.
8
A toll for T cell costimulation.T细胞共刺激的代价。
Ann Rheum Dis. 2004 Nov;63 Suppl 2(Suppl 2):ii76-ii78. doi: 10.1136/ard.2004.028308.
9
Protection against systemic candidiasis in mice immunized with secreted aspartic proteinase 2.用分泌型天冬氨酸蛋白酶2免疫的小鼠对系统性念珠菌病的保护作用。
Immunology. 2004 Mar;111(3):334-42. doi: 10.1111/j.1365-2567.2004.01819.x.
10
TLR2 is expressed on activated T cells as a costimulatory receptor.Toll样受体2(TLR2)作为共刺激受体在活化的T细胞上表达。
Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3029-34. doi: 10.1073/pnas.0400171101. Epub 2004 Feb 23.