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人孕早期蜕膜中CD56 + 淋巴细胞作为新型转化生长因子-β2相关免疫抑制因子的来源

CD56+ lymphoid cells in human first trimester pregnancy decidua as a source of novel transforming growth factor-beta 2-related immunosuppressive factors.

作者信息

Clark D A, Vince G, Flanders K C, Hirte H, Starkey P

机构信息

Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

出版信息

Hum Reprod. 1994 Dec;9(12):2270-7. doi: 10.1093/oxfordjournals.humrep.a138436.

Abstract

The lymphomyeloid cells isolated from normal first trimester pregnancy decidua may be separated into a CD56+ population of natural killer (NK)-lineage cells with the morphology of granulated lymphocytes, and a CD56- population which includes other cell types. Unlike CD56+ NK cells in peripheral blood, decidual CD56+ cells lack type III Fc receptors (CD16) and did not express significant levels of either type I FcR (CD64) or type II FcR (CDw32). By contrast to the decidual CD56- cells, CD56+ cells could release biologically active transforming growth factor (TGF)-beta in vitro, detectable using an normal rat kidney fibroblast colony-forming assay. The CD56+ cells could be stained using an antibody specific for TGF-beta 2, and similarly staining cells could be detected in intact biopsies of normal pregnancy decidua. Bioactive TGF-beta is known to suppress the generation of cytotoxic cells in vitro, and high performance liquid chromatography fractionation of supernatants conditioned by CD56+ but not CD56- cells contained reproducible peaks of immunosuppressive activity at 40-45 and 15-20 kDa, similar to the TGF-beta 2 immunosuppressive activity in supernatants conditioned by unfractionated decidua.

摘要

从正常孕早期蜕膜中分离出的淋巴髓样细胞可分为具有颗粒淋巴细胞形态的自然杀伤(NK)细胞系的CD56 +群体,以及包含其他细胞类型的CD56 -群体。与外周血中的CD56 + NK细胞不同,蜕膜CD56 +细胞缺乏III型Fc受体(CD16),且不表达显著水平的I型FcR(CD64)或II型FcR(CDw32)。与蜕膜CD56 -细胞相比,CD56 +细胞在体外可释放具有生物活性的转化生长因子(TGF)-β,可使用正常大鼠肾成纤维细胞集落形成试验检测到。CD56 +细胞可用针对TGF-β2的特异性抗体染色,在正常妊娠蜕膜的完整活检组织中也可检测到类似染色的细胞。已知生物活性TGF-β在体外可抑制细胞毒性细胞的产生,由CD56 +而非CD56 -细胞培养上清液经高效液相色谱分离后,在40 - 45 kDa和15 - 20 kDa处含有可重复的免疫抑制活性峰,类似于未分级蜕膜培养上清液中的TGF-β2免疫抑制活性。

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