• 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

麻风的皮肤浸润:细胞特征及主要T细胞表型

The cutaneous infiltrates of leprosy: cellular characteristics and the predominant T-cell phenotypes.

作者信息

Van Voorhis W C, Kaplan G, Sarno E N, Horwitz M A, Steinman R M, Levis W R, Nogueira N, Hair L S, Gattass C R, Arrick B A, Cohn Z A

出版信息

N Engl J Med. 1982 Dec 23;307(26):1593-7. doi: 10.1056/NEJM198212233072601.

DOI:10.1056/NEJM198212233072601
PMID:6216407
Abstract

We report on the characteristics of cells in the cutaneous lesions and blood of 21 patients with lepromatous, tuberculoid, and intermediate forms of leprosy. A large proportion of the infiltrates in lepromatous lesions consist of macrophages heavily parasitized with Mycobacterium leprae. The T cells in the lesions are devoid of OKT4/Leu 3a-positive ("helper") cells and consist almost exclusively of OKT8/Leu 2a-positive ("suppressor") populations. In contrast, the tuberculoid infiltrates contain well-organized epithelioid and giant-cell granulomas and only remnants of bacilli, and the predominant T cell is from the OKT4/Leu 3a-positive subset. In both tuberculoid and lepromatous infiltrates, T cells and macrophages expressed HLA-DR antigen. No marked alteration in the distribution of blood T-cell phenotypes was noted. We conclude that there is a marked difference between T-cell subsets in lepromatous and tuberculoid infiltrates, which may influence the microbicidal activity of macrophages in the lesions.

摘要

我们报告了21例瘤型、结核样型及中间型麻风患者皮肤损害处及血液中的细胞特征。瘤型损害中的大量浸润细胞由被麻风杆菌严重寄生的巨噬细胞组成。损害处的T细胞缺乏OKT4/Leu 3a阳性(“辅助性”)细胞,几乎完全由OKT8/Leu 2a阳性(“抑制性”)群体组成。相比之下,结核样浸润含有组织良好的上皮样细胞和巨细胞肉芽肿,仅残留少量杆菌,且主要的T细胞来自OKT4/Leu 3a阳性亚群。在结核样和瘤型浸润中,T细胞和巨噬细胞均表达HLA-DR抗原。血液T细胞表型分布未发现明显改变。我们得出结论,瘤型和结核样浸润中的T细胞亚群存在显著差异,这可能会影响损害处巨噬细胞的杀菌活性。

相似文献

1
The cutaneous infiltrates of leprosy: cellular characteristics and the predominant T-cell phenotypes.麻风的皮肤浸润:细胞特征及主要T细胞表型
N Engl J Med. 1982 Dec 23;307(26):1593-7. doi: 10.1056/NEJM198212233072601.
2
Differences in predominant T cell phenotypes and distribution pattern in reactional lesions of tuberculoid and lepromatous leprosy.结核样型和瘤型麻风反应性损害中主要T细胞表型及分布模式的差异。
Clin Exp Immunol. 1984 Mar;55(3):623-8.
3
T cell subsets in leprosy lesions: in situ characterization using monoclonal antibodies.麻风病损中的T细胞亚群:使用单克隆抗体的原位特征分析
Clin Exp Immunol. 1983 Mar;51(3):421-9.
4
Cloned suppressor T cells from a lepromatous leprosy patient suppress Mycobacterium leprae reactive helper T cells.从一名瘤型麻风患者身上克隆出的抑制性T细胞可抑制麻风分枝杆菌反应性辅助性T细胞。
Nature. 1986;322(6078):462-4. doi: 10.1038/322462a0.
5
A follow up of T-cell subsets and of anti-M. leprae antibody titer as measured by the FLA-ABS test in Melanesian leprosy patients under polychemotherapy.对接受多药化疗的美拉尼西亚麻风患者,通过荧光麻风抗体吸收试验(FLA-ABS)测定其T细胞亚群和抗麻风杆菌抗体滴度的随访研究。
Int J Lepr Other Mycobact Dis. 1986 Mar;54(1):38-45.
6
In vivo responses to Mycobacterium leprae: antigen presentation, interleukin-2 production, and immune cell phenotypes in naturally occurring leprosy lesions.对麻风分枝杆菌的体内反应:自然发生的麻风病损中的抗原呈递、白细胞介素-2产生及免疫细胞表型
Int J Lepr Other Mycobact Dis. 1985 Sep;53(3):385-94.
7
Genetically restricted suppressor T-cell clones derived from lepromatous leprosy lesions.源自瘤型麻风病损的基因受限抑制性T细胞克隆。
Nature. 1986;322(6078):459-61. doi: 10.1038/322459a0.
8
In vitro studies on dermal granulomas of human leprosy: characterization of cells using monoclonal antibodies.人类麻风病皮肤肉芽肿的体外研究:使用单克隆抗体对细胞进行表征
Int J Lepr Other Mycobact Dis. 1986 Jun;54(2):268-72.
9
In situ characterization of T lymphocyte subsets in the reactional states of leprosy.麻风反应状态下T淋巴细胞亚群的原位特征分析
Clin Exp Immunol. 1983 Jul;53(1):17-24.
10
In situ identification of activated Ta1+ T lymphocytes in human leprosy skin lesions.人麻风皮肤病变中活化Ta1 + T淋巴细胞的原位鉴定。
Int J Lepr Other Mycobact Dis. 1987 Sep;55(3):494-8.

引用本文的文献

1
Leptin Deficiency May Influence the Divergence of Cell-Mediated Immunity Between Lepromatous and Tuberculoid Leprosy Patients.瘦素缺乏可能影响瘤型和结核样型麻风患者细胞介导免疫的差异。
J Inflamm Res. 2022 Dec 13;15:6719-6728. doi: 10.2147/JIR.S389845. eCollection 2022.
2
IL-26 contributes to host defense against intracellular bacteria.白细胞介素-26 有助于宿主抵御细胞内细菌。
J Clin Invest. 2019 Apr 2;129(5):1926-1939. doi: 10.1172/JCI99550.
3
Distinct regions of the large extracellular domain of tetraspanin CD9 are involved in the control of human multinucleated giant cell formation.
四跨膜蛋白CD9大细胞外结构域的不同区域参与对人多核巨细胞形成的调控。
PLoS One. 2014 Dec 31;9(12):e116289. doi: 10.1371/journal.pone.0116289. eCollection 2014.
4
Differential dermal expression of CCL17 and CCL18 in tuberculoid and lepromatous leprosy.CCL17和CCL18在结核样型和瘤型麻风病中的皮肤差异表达
PLoS Negl Trop Dis. 2014 Nov 20;8(11):e3263. doi: 10.1371/journal.pntd.0003263. eCollection 2014.
5
Leprosy: review of the epidemiological, clinical, and etiopathogenic aspects - part 1.麻风病:流行病学、临床及病因学方面综述 - 第1部分
An Bras Dermatol. 2014 Mar-Apr;89(2):205-18. doi: 10.1590/abd1806-4841.20142450.
6
Atypical erythema nodosum leprosum as the presenting feature in multibacillary leprosy: a case report.非典型结节性麻风红斑作为多菌型麻风的首发表现:一例报告
Indian J Dermatol. 2014 Jan;59(1):94-5. doi: 10.4103/0019-5154.123519.
7
A journey in science: promise, purpose, privilege.科学之旅:承诺、目标、特权。
Mol Med. 2013 Oct 3;19(1):305-13. doi: 10.2119/molmed.2013.00063.
8
Leprosy: an overview of pathophysiology.麻风病:病理生理学概述
Interdiscip Perspect Infect Dis. 2012;2012:181089. doi: 10.1155/2012/181089. Epub 2012 Sep 4.
9
Mycobacterium leprae-host-cell interactions and genetic determinants in leprosy: an overview.麻风分枝杆菌与麻风宿主细胞的相互作用及其遗传决定因素:概述。
Future Microbiol. 2011 Feb;6(2):217-30. doi: 10.2217/fmb.10.173.
10
Changes in expression of signal transduction proteins in T lymphocytes of patients with leprosy.麻风病患者T淋巴细胞中信号转导蛋白表达的变化
Infect Immun. 1998 Feb;66(2):499-504. doi: 10.1128/IAI.66.2.499-504.1998.