• 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

蕈样肉芽肿皮肤病变含有表达活化的、MHC限制的细胞毒性T淋巴细胞表型的CD8 +肿瘤浸润淋巴细胞。

Mycosis fungoides skin lesions contain CD8+ tumor-infiltrating lymphocytes expressing an activated, MHC-restricted cytotoxic T-lymphocyte phenotype.

作者信息

Wood G S, Edinger A, Hoppe R T, Warnke R A

机构信息

Department of Dermatology, Case Western Reserve University, Cleveland, OH.

出版信息

J Cutan Pathol. 1994 Apr;21(2):151-6. doi: 10.1111/j.1600-0560.1994.tb00250.x.

DOI:10.1111/j.1600-0560.1994.tb00250.x
PMID:8040463
Abstract

In prior studies, we showed that most CD8+ cells infiltrating skin lesions of CD3+CD4+ mycosis fungoides were CD3+ T-lineage tumor-infiltrating lymphocytes (TIL) whose overall phenotype was suggestive of MHC-restricted cytotoxic T lymphocytes (CTL). However, their lack of cytotoxic-associated granzyme A mRNA suggested that they might be unactivated CTL precursors. In this study, we used single- and double-label immunohistologic techniques to assess the expression of TIA-1-reactive protein and HLA-DR by these CD8+TIL. Monoclonal antibody TIA-1 recognizes a novel family of proteins expressed preferentially by cytotoxic cells, including some that lack granzyme A. HLA-DR is a marker of T-cell activation. Single-label studies of 32 cases showed that CD8+TIL and TIA-1+ cells constituted a variable minority of the total cellular infiltrate and had a similar distribution. Double-label studies of 14 cases showed that in most instances the aggregate phenotype of the majority of CD8+TIL was CD3+TIA-1+HLA-DR+CD56-CD57-. These findings suggest that many of the CD8+TIL within skin lesions of CD3+CD4+ mycosis fungoides are activated, MHC-restricted CTL.

摘要

在先前的研究中,我们发现浸润于CD3 + CD4 + 蕈样肉芽肿皮肤病变中的大多数CD8 + 细胞是CD3 + T细胞谱系肿瘤浸润淋巴细胞(TIL),其总体表型提示为MHC限制性细胞毒性T淋巴细胞(CTL)。然而,它们缺乏细胞毒性相关的颗粒酶A mRNA,这表明它们可能是未活化的CTL前体。在本研究中,我们使用单标记和双标记免疫组织学技术来评估这些CD8 + TIL中TIA - 1反应蛋白和HLA - DR的表达。单克隆抗体TIA - 1识别一类优先由细胞毒性细胞表达的新蛋白家族,包括一些缺乏颗粒酶A的蛋白。HLA - DR是T细胞活化的标志物。对32例病例的单标记研究表明,CD8 + TIL和TIA - 1 + 细胞占总细胞浸润的可变少数,且分布相似。对14例病例的双标记研究表明,在大多数情况下,大多数CD8 + TIL的聚集表型为CD3 + TIA - 1 + HLA - DR + CD56 - CD57 - 。这些发现表明,CD3 + CD4 + 蕈样肉芽肿皮肤病变中的许多CD8 + TIL是活化的、MHC限制性CTL。

相似文献

1
Mycosis fungoides skin lesions contain CD8+ tumor-infiltrating lymphocytes expressing an activated, MHC-restricted cytotoxic T-lymphocyte phenotype.蕈样肉芽肿皮肤病变含有表达活化的、MHC限制的细胞毒性T淋巴细胞表型的CD8 +肿瘤浸润淋巴细胞。
J Cutan Pathol. 1994 Apr;21(2):151-6. doi: 10.1111/j.1600-0560.1994.tb00250.x.
2
Most CD8+ cells in skin lesions of CD3+ CD4+ mycosis fungoides are CD3+ T cells that lack CD11b, CD16, CD56, CD57, and human Hanukah factor mRNA.在CD3+ CD4+蕈样肉芽肿皮肤病变中的大多数CD8+细胞是缺乏CD11b、CD16、CD56、CD57和人哈努卡因子mRNA的CD3+ T细胞。
Am J Pathol. 1991 Jun;138(6):1545-52.
3
Tumor specific cytolysis by tumor infiltrating lymphocytes in breast cancer.乳腺癌中肿瘤浸润淋巴细胞介导的肿瘤特异性细胞溶解作用。
Cancer. 1994 Aug 15;74(4):1275-82. doi: 10.1002/1097-0142(19940815)74:4<1275::aid-cncr2820740416>3.0.co;2-q.
4
Phenotype, cytokine production and cytolytic capacity of fresh (uncultured) tumour-infiltrating T lymphocytes in human renal cell carcinoma.人肾细胞癌中新鲜(未培养)肿瘤浸润性T淋巴细胞的表型、细胞因子产生及细胞溶解能力
Clin Exp Immunol. 1997 Sep;109(3):501-9. doi: 10.1046/j.1365-2249.1997.4771375.x.
5
Progression of mycosis fungoides occurs through divergence of tumor immunophenotype by differential expression of HLA-DR.蕈样肉芽肿的进展是通过 HLA-DR 的差异表达导致肿瘤免疫表型的分歧。
Blood Adv. 2019 Feb 26;3(4):519-530. doi: 10.1182/bloodadvances.2018025114.
6
Immunohistochemical analysis of mycosis fungoides on paraffin-embedded tissue sections.石蜡包埋组织切片上蕈样肉芽肿的免疫组织化学分析
Mod Pathol. 1998 Oct;11(10):978-82.
7
[Lymphocyte activation markers in patients with ovarian cancer].[卵巢癌患者的淋巴细胞活化标志物]
Ginekol Pol. 2012 Oct;83(10):737-43.
8
Crosstalk between tumor T lymphocytes and reactive T lymphocytes in cutaneous T cell lymphomas.皮肤T细胞淋巴瘤中肿瘤性T淋巴细胞与反应性T淋巴细胞之间的串扰。
Ann N Y Acad Sci. 2001 Sep;941:31-8. doi: 10.1111/j.1749-6632.2001.tb03708.x.
9
The immunophenotype and activation status of the lymphocytic infiltrate in human breast cancers, the role of the major histocompatibility complex in cell-mediated immune mechanisms, and their association with prognostic indicators.人类乳腺癌中淋巴细胞浸润的免疫表型和激活状态、主要组织相容性复合体在细胞介导免疫机制中的作用及其与预后指标的关联。
Surgery. 2003 Nov;134(5):827-34. doi: 10.1016/s0039-6060(03)00292-7.
10
Cytotoxic potential despite impaired activation pathways in T lymphocytes infiltrating nasopharyngeal carcinoma.尽管浸润鼻咽癌的T淋巴细胞激活途径受损,但其仍具有细胞毒性潜力。
Int J Cancer. 1991 Feb 1;47(3):362-70. doi: 10.1002/ijc.2910470309.

引用本文的文献

1
Malignant and Benign T Cells Constituting Cutaneous T-Cell Lymphoma.构成皮肤 T 细胞淋巴瘤的恶性和良性 T 细胞。
Int J Mol Sci. 2021 Nov 29;22(23):12933. doi: 10.3390/ijms222312933.
2
Cellular Interactions and Inflammation in the Pathogenesis of Cutaneous T-Cell Lymphoma.皮肤T细胞淋巴瘤发病机制中的细胞相互作用与炎症
Front Cell Dev Biol. 2020 Sep 4;8:851. doi: 10.3389/fcell.2020.00851. eCollection 2020.
3
Malignant inflammation in cutaneous T-cell lymphoma-a hostile takeover.皮肤T细胞淋巴瘤中的恶性炎症——一场恶意接管。
Semin Immunopathol. 2017 Apr;39(3):269-282. doi: 10.1007/s00281-016-0594-9. Epub 2016 Oct 7.
4
The influence of the coexpression of CD4 and CD8 in cutaneous lesions on prognosis of mycosis fungoides: a preliminary study.皮肤病变中CD4和CD8共表达对蕈样肉芽肿预后的影响:一项初步研究。
J Skin Cancer. 2014;2014:624143. doi: 10.1155/2014/624143. Epub 2014 Jul 20.
5
Evolving insights in the pathogenesis and therapy of cutaneous T-cell lymphoma (mycosis fungoides and Sezary syndrome).皮肤 T 细胞淋巴瘤(蕈样肉芽肿和赛泽里综合征)发病机制和治疗中不断发展的认识。
Br J Haematol. 2011 Oct;155(2):150-66. doi: 10.1111/j.1365-2141.2011.08852.x. Epub 2011 Aug 25.
6
Sézary T-cell activating factor is a Chlamydia pneumoniae-associated protein.塞扎里T细胞激活因子是一种与肺炎衣原体相关的蛋白质。
Clin Diagn Lab Immunol. 1999 Nov;6(6):895-905. doi: 10.1128/CDLI.6.6.895-905.1999.