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朗格汉斯细胞组织细胞增生症病灶中的 Foxp3+ Tregs 共表达 CD56,且具有明确的调节能力。

Foxp3 Tregs from Langerhans cell histiocytosis lesions co-express CD56 and have a definitively regulatory capacity.

机构信息

Fiona Elsey Cancer Research Institute, Ballarat, Australia; Federation University Australia, Ballarat, Australia.

Childhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden; Karolinska University Hospital, Stockholm, Sweden.

出版信息

Clin Immunol. 2020 Jun;215:108418. doi: 10.1016/j.clim.2020.108418. Epub 2020 Apr 10.

DOI:10.1016/j.clim.2020.108418
PMID:32283322
Abstract

Langerhans cell histiocytosis (LCH) lesions contain myeloid lineage 'LCH' cells. Regulatory T cells (Tregs) are also enriched within lesions, although their role in LCH pathogenesis is unknown. LCH cells are thought to produce the transforming growth factor beta (TGF-β) within lesions, however whether Tregs contribute is unestablished. Using flow cytometry, we analyzed relative frequencies of live Tregs from LCH patients and identified CD56 expression and TGF-β production by lesion Tregs. While CD56 Tregs were enriched in lesions, overall CD56 T cells were reduced in the blood from active LCH patients compared to non-active disease patients, and there was a negative correlation between CD8CD56 T cells and Tregs. We propose that inducing a Treg phenotype in T cells such as CD56 T cells may be a mechanism by which LCH cells divert inflammatory T cell responses. Thus, Tregs within LCH lesions are likely an important component in LCH pathogenesis.

摘要

朗格汉斯细胞组织细胞增生症 (LCH) 病变包含髓系“LCH”细胞。调节性 T 细胞 (Tregs) 在病变中也丰富存在,尽管它们在 LCH 发病机制中的作用尚不清楚。LCH 细胞被认为在病变中产生转化生长因子-β (TGF-β),然而 Tregs 是否有贡献尚不确定。通过流式细胞术,我们分析了 LCH 患者活 Tregs 的相对频率,并鉴定了病变 Tregs 的 CD56 表达和 TGF-β 产生。虽然 CD56 Tregs 在病变中丰富存在,但与非活动疾病患者相比,活性 LCH 患者的血液中总 CD56 T 细胞减少,并且 CD8CD56 T 细胞与 Tregs 之间呈负相关。我们提出,在 T 细胞(如 CD56 T 细胞)中诱导 Treg 表型可能是 LCH 细胞转移炎症性 T 细胞反应的一种机制。因此,LCH 病变中的 Tregs 可能是 LCH 发病机制中的一个重要组成部分。

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