Transcriptional repression shapes the identity and function of tissue macrophages.
Transcriptional repression shapes the identity and function of tissue macrophages.
复制标题
DOI:
10.1002/2211-5463.13269
复制
发表时间:
2021-12
期刊:
影响因子:
2.6
通讯作者:
Nagy L
中科院分区:
文献类型:
--
作者:
Bene K;Halasz L;Nagy L
The changing extra‐ and intracellular microenvironment calls for rapid cell fate decisions that are precisely and primarily regulated at the transcriptional level. The cellular components of the immune system are excellent examples of how cells respond and adapt to different environmental stimuli. Innate immune cells such as macrophages are able to modulate their transcriptional programs and epigenetic regulatory networks through activation and repression of particular genes, allowing them to quickly respond to a rapidly changing environment. Tissue macrophages are essential components of different immune‐ and nonimmune cell‐mediated physiological mechanisms in mammals and are widely used models for investigating transcriptional regulatory mechanisms. Therefore, it is critical to unravel the distinct sets of transcription activators, repressors, and coregulators that play roles in determining tissue macrophage identity and functions during homeostasis, as well as in diseases affecting large human populations, such as metabolic syndromes, immune‐deficiencies, and tumor development. In this review, we will focus on transcriptional repressors that play roles in tissue macrophage development and function under physiological conditions. Tissue macrophages are essential cellular components in maintaining tissue homeostasis and integrity through their effector functions. Tissue‐resident macrophages such as the alveolar, splenic red pulp, intestinal macrophages, and microglia have overlapping function. The identity and function of tissue‐resident macrophage subtypes are orchestrated by distinct sets of transcriptional activator and repressor proteins. In this review, we focus on repressors.
登录
查看更多内容
影响因子:
64.5
作者:
Haldar M;Kohyama M;So AY;Kc W;Wu X;Briseño CG;Satpathy AT;Kretzer NM;Arase H;Rajasekaran NS;Wang L;Egawa T;Igarashi K;Baltimore D;Murphy TL;Murphy KM
通讯作者:
Murphy KM
影响因子:
5.2
作者:
Czimmerer Z;Halasz L;Nagy L
通讯作者:
Nagy L
影响因子:
29
作者:
Barish GD;Yu RT;Karunasiri MS;Becerra D;Kim J;Tseng TW;Tai LJ;Leblanc M;Diehl C;Cerchietti L;Miller YI;Witztum JL;Melnick AM;Dent AL;Tangirala RK;Evans RM
通讯作者:
Evans RM
影响因子:
64.5
作者:
Gosselin D;Link VM;Romanoski CE;Fonseca GJ;Eichenfield DZ;Spann NJ;Stender JD;Chun HB;Garner H;Geissmann F;Glass CK
通讯作者:
Glass CK
影响因子:
8.7
作者:
Bain CC;Mowat AM
通讯作者:
Mowat AM