近日，德国雷根斯堡大学Markus Feuerer及其研究组发现，非淋巴组织调节性T（Treg）细胞的前体存在于次级淋巴器官中，并由转录因子BATF调控。该研究2020年1月7日在线发表于国际学术期刊《免疫》。

使用转录因子核因子、白介素3调节（Nfil3）的报告小鼠和单细胞RNA测序（scRNA-seq），研究人员确定了表达白介素33（IL-33）受体ST2的非淋巴组织Treg细胞的两个前体阶段，其驻留在脾和淋巴结中。非淋巴组织Treg细胞和两个前体阶段的整体染色质分析揭示了染色质可及性的逐步获取，并朝着非淋巴组织Treg细胞表型重编程。从机制上讲，研究人员确定并验证了转录因子Batf作为前体细胞分子组织程序的驱动因子。了解该组织发育程序将有助于利用组织Treg细胞的再生特性进行治疗。

据介绍，专门的reg细胞在非淋巴组织中积聚并执行体内平衡和再生功能。是否存在非淋巴组织Treg细胞的共同前体以及它们如何分化仍然不清楚。

附：英文原文

Title: Precursors for Nonlymphoid-Tissue Treg Cells Reside in Secondary Lymphoid Organs and Are Programmed by the Transcription Factor BATF

Author: Michael Delacher, Charles D. Imbusch, Agnes Hotz-Wagenblatt, Jan-Philipp Mallm, Katharina Bauer, Malte Simon, Dania Riegel, André F. Rendeiro, Sebastian Bittner, Lieke Sanderink, Asmita Pant, Lisa Schmidleithner, Kathrin L. Braband, Bernd Echtenachter, Alexander Fischer, Valentina Giunchiglia, Petra Hoffmann, Matthias Edinger, Christoph Bock, Michael Rehli, Benedikt Brors, Christian Schmidl, Markus Feuerer

Issue&Volume: January 7, 2020

Abstract: Specialized regulatory T (Treg) cells accumulate and perform homeostatic and regenerative functions in nonlymphoid tissues. Whether common precursors for nonlymphoid-tissue Treg cells exist and how they differentiate remain elusive. Using transcription factor nuclear factor, interleukin 3 regulated (Nfil3) reporter mice and single-cell RNA-sequencing (scRNA-seq), we identified two precursor stages of interleukin 33 (IL-33) receptor ST2-expressing nonlymphoid tissue Treg cells, which resided in the spleen and lymph nodes. Global chromatin profiling of nonlymphoid tissue Treg cells and the two precursor stages revealed a stepwise acquisition of chromatin accessibility and reprogramming toward the nonlymphoid-tissue Treg cell phenotype. Mechanistically, we identified and validated the transcription factor Batf as the driver of the molecular tissue program in the precursors. Understanding this tissue development program will help to harness regenerative properties of tissue Treg cells for therapy.

DOI: 10.1016/j.immuni.2019.12.002

Source: https://www.cell.com/immunity/fulltext/S1074-7613(19)30498-4