• 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

小鼠感染大鼠类圆线虫过程中淋巴细胞产生肥大细胞生长因子的动力学研究。

Kinetic study of mast-cell growth factor production by lymphocytes during the course of Strongyloides ratti infection in mice.

作者信息

Abe T, Nawa Y

机构信息

Department of Parasitology, Miyazaki Medical College, Japan.

出版信息

Parasitol Res. 1988;74(5):484-8. doi: 10.1007/BF00535150.

DOI:10.1007/BF00535150
PMID:3261861
Abstract

Mast-cell growth factor (MCGF) activity in the media conditioned by mesenteric lymph node or spleen cells from Strongyloides ratti-infected C57BL/6 mice was examined by using factor-dependent cell line FDC-P2 or bone marrow-derived, cultured mast cells (BMMC) as indicators. Mesenteric lymph node cells from infected mice spontaneously released MCGF activity by culturing for 24 h, showing peak production on days 5-7. MCGF production by mesenteric lymph node cells was augmented after stimulation with adult worm antigen or with concanavalin A (con A). The peak of MCGF production by antigen-stimulated lymph node cells was observed on days 5-7 and declined thereafter. MCGF production by antigen-stimulated spleen cells was lower than that by lymph node cells and reached a peak on day 7 or later. Normal lymph node or spleen cells did not produce MCGF activity even after stimulation with adult worm antigen. The peak of MCGF production by mesenteric lymph node cells preceded the peak of intestinal mastocytosis at the infected site by 4-6 days. The cells producing MCGF had a phenotype of Thy-1+, L3T4+, and Lyt-2-. The possible importance of mucosal mast cells in worm expulsion is discussed.

摘要

利用依赖因子的细胞系FDC - P2或骨髓来源的培养肥大细胞(BMMC)作为指标,检测了来自感染大鼠类圆线虫的C57BL/6小鼠肠系膜淋巴结或脾细胞所产生的培养基中的肥大细胞生长因子(MCGF)活性。感染小鼠的肠系膜淋巴结细胞通过培养24小时可自发释放MCGF活性,在第5 - 7天产量达到峰值。用成虫抗原或伴刀豆球蛋白A(cona)刺激后,肠系膜淋巴结细胞的MCGF产量增加。抗原刺激的淋巴结细胞产生MCGF的峰值在第5 - 7天出现,随后下降。抗原刺激的脾细胞产生的MCGF低于淋巴结细胞,且在第7天或更晚达到峰值。正常淋巴结或脾细胞即使在用成虫抗原刺激后也不产生MCGF活性。肠系膜淋巴结细胞产生MCGF的峰值比感染部位肠道肥大细胞增多的峰值提前4 - 6天。产生MCGF的细胞具有Thy - 1 +、L3T4 +和Lyt - 2 -的表型。本文讨论了黏膜肥大细胞在驱蠕虫过程中可能的重要性。

相似文献

1
Kinetic study of mast-cell growth factor production by lymphocytes during the course of Strongyloides ratti infection in mice.小鼠感染大鼠类圆线虫过程中淋巴细胞产生肥大细胞生长因子的动力学研究。
Parasitol Res. 1988;74(5):484-8. doi: 10.1007/BF00535150.
2
Analysis of T cell populations and IL-3 mRNA expression in mesenteric lymph node cells and intestinal intraepithelial lymphocytes in Strongyloides ratti-infected mice.感染大鼠类圆线虫的小鼠肠系膜淋巴结细胞和肠上皮内淋巴细胞中T细胞群体及IL-3 mRNA表达的分析
J Helminthol. 1998 Mar;72(1):1-8. doi: 10.1017/s0022149x00000894.
3
Reconstitution of mucosal mast cells in W/WV mice by adoptive transfer of bone marrow-derived cultured mast cells and its effects on the protective capacity to Strongyloides ratti-infection.
Parasite Immunol. 1987 Jan;9(1):31-8. doi: 10.1111/j.1365-3024.1987.tb00486.x.
4
The effect of interleukin-4 on the induction of intestinal mast cells and chronological cytokine profiles during intestinal nematode Strongyloides ratti infection.白细胞介素-4对肠道线虫类圆线虫感染期间肠道肥大细胞诱导及细胞因子时间序列谱的影响。
Parasitol Res. 2001 Feb;87(2):149-54. doi: 10.1007/pl00008568.
5
Localization of mucosal mast cells in W/Wv mice after reconstitution with bone marrow cells or cultured mast cells, and its relation to the protective capacity to Strongyloides ratti infection.用骨髓细胞或培养的肥大细胞重建后W/Wv小鼠黏膜肥大细胞的定位及其与抗鼠类圆线虫感染保护能力的关系。
Parasite Immunol. 1987 Jul;9(4):477-85. doi: 10.1111/j.1365-3024.1987.tb00524.x.
6
Intestinal protection against Strongyloides ratti and mastocytosis induced by administration of interleukin-3 in mice.白细胞介素-3给药对小鼠肠道抗鼠类圆线虫及肥大细胞增多症的保护作用。
Immunology. 1993 Sep;80(1):116-21.
7
Early increase of gut intraepithelial mast cell precursors following Strongyloides venezuelensis infection in mice.委内瑞拉类圆线虫感染小鼠后肠道上皮内肥大细胞前体细胞的早期增加
Parasitology. 1997 Feb;114 ( Pt 2):181-7. doi: 10.1017/s0031182096008384.
8
Immunity to Strongyloides ratti in rats. 1. Adoptive transfer with mesenteric lymph node cells.大鼠对鼠类圆线虫的免疫。1. 肠系膜淋巴结细胞的过继转移。
Parasite Immunol. 1981 Autumn;3(3):181-9. doi: 10.1111/j.1365-3024.1981.tb00397.x.
9
Transfer by serum and cells of resistance to infection with Strongyloides ratti in mice.通过血清和细胞传递小鼠对大鼠类圆线虫感染的抵抗力。
Immunology. 1981 Jun;43(2):317-22.
10
Defective protective capacity of W/Wv mice against Strongyloides ratti infection and its reconstitution with bone marrow cells.W/Wv小鼠对鼠类圆线虫感染的保护性能力缺陷及其骨髓细胞重建
Parasite Immunol. 1985 Jul;7(4):429-38. doi: 10.1111/j.1365-3024.1985.tb00088.x.

引用本文的文献

1
Adolescent Idiopathic Scoliosis: Advances in Diagnosis and Management.青少年特发性脊柱侧弯:诊断与治疗进展
Curr Rev Musculoskelet Med. 2025 Feb;18(2):54-60. doi: 10.1007/s12178-024-09939-2. Epub 2024 Dec 30.
2
NIP45 controls the magnitude of the type 2 T helper cell response.NIP45 控制 2 型辅助性 T 细胞应答的幅度。
Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3663-8. doi: 10.1073/pnas.0914700107. Epub 2010 Feb 4.
3
Major histocompatibility complex (MHC) class II but not MHC class I molecules are required for efficient control of Strongyloides venezuelensis infection in mice.

本文引用的文献

1
Strongyloides ratti: mast cell and goblet cell responses in the small intestine of infected rats.
Exp Parasitol. 1982 Dec;54(3):366-70. doi: 10.1016/0014-4894(82)90045-5.
2
Immunologic responses to experimental strongyloidiasis in rats.大鼠实验性类圆线虫病的免疫反应。
Z Parasitenkd. 1983;69(5):667-75. doi: 10.1007/BF00926676.
3
Mucosal mast cells are functionally active during spontaneous expulsion of intestinal nematode infections in rat.在大鼠肠道线虫感染的自发排出过程中,黏膜肥大细胞具有功能活性。
主要组织相容性复合体 (MHC) Ⅱ类分子而非 MHC Ⅰ类分子是控制委内瑞拉旋毛虫感染的关键。
Immunology. 2009 Sep;128(1 Suppl):e432-41. doi: 10.1111/j.1365-2567.2008.02995.x. Epub 2008 Dec 16.
4
Role of phosphoinositide 3-kinase signaling in mast cells: new insights from knockout mouse studies.磷酸肌醇3-激酶信号通路在肥大细胞中的作用:基因敲除小鼠研究的新见解
J Mol Med (Berl). 2003 Sep;81(9):524-35. doi: 10.1007/s00109-003-0475-2. Epub 2003 Aug 19.
5
Intestinal protection against Strongyloides ratti and mastocytosis induced by administration of interleukin-3 in mice.白细胞介素-3给药对小鼠肠道抗鼠类圆线虫及肥大细胞增多症的保护作用。
Immunology. 1993 Sep;80(1):116-21.
Nature. 1984;312(5993):450-2. doi: 10.1038/312450a0.
4
Gut mucosal mast cells. Origin, traffic, and differentiation.肠道黏膜肥大细胞。起源、迁移与分化。
J Exp Med. 1984 Jul 1;160(1):12-28. doi: 10.1084/jem.160.1.12.
5
Biologic properties of homogeneous interleukin 3. I. Demonstration of WEHI-3 growth factor activity, mast cell growth factor activity, p cell-stimulating factor activity, colony-stimulating factor activity, and histamine-producing cell-stimulating factor activity.同源白细胞介素3的生物学特性。I. WEHI-3生长因子活性、肥大细胞生长因子活性、β细胞刺激因子活性、集落刺激因子活性及组胺产生细胞刺激因子活性的证明。
J Immunol. 1983 Jul;131(1):282-7.
6
Immune reactions in mucous membranes. I. Intestinal mast cell response during helminth expulsion in the rat.黏膜中的免疫反应。I. 大鼠驱蠕虫过程中肠道肥大细胞的反应。
Immunology. 1971 Mar;20(3):277-88.
7
In vitro generated mast cells express natural cytotoxicity against tumour cells.体外培养生成的肥大细胞对肿瘤细胞表现出天然细胞毒性。
Immunology. 1985 Jun;55(2):317-24.
8
Defective protective capacity of W/Wv mice against Strongyloides ratti infection and its reconstitution with bone marrow cells.W/Wv小鼠对鼠类圆线虫感染的保护性能力缺陷及其骨髓细胞重建
Parasite Immunol. 1985 Jul;7(4):429-38. doi: 10.1111/j.1365-3024.1985.tb00088.x.
9
Reconstitution of mucosal mast cells in W/WV mice by adoptive transfer of bone marrow-derived cultured mast cells and its effects on the protective capacity to Strongyloides ratti-infection.
Parasite Immunol. 1987 Jan;9(1):31-8. doi: 10.1111/j.1365-3024.1987.tb00486.x.
10
Characterization of a murine lymphokine distinct from interleukin 2 and interleukin 3 (IL-3) possessing a T-cell growth factor activity and a mast-cell growth factor activity that synergizes with IL-3.一种不同于白细胞介素2和白细胞介素3(IL-3)的小鼠淋巴因子的特性,该淋巴因子具有T细胞生长因子活性和与IL-3协同作用的肥大细胞生长因子活性。
Proc Natl Acad Sci U S A. 1986 Mar;83(6):1857-61. doi: 10.1073/pnas.83.6.1857.