发布时间:
2021-04-27 00:00:00
期刊:
PNAS
doi: 10.1073/pnas.2023172118
作者:
Chiara Bernardi,Gaëtan Maurer,Tao Ye,Patricia Marchal,Bernard Jost,Manuela Wissler,Ulrich Maurer,Philippe Kastner,Susan Chan,Céline Charvet
摘要:
The production of proinflammatory cytokines, particularly granulocyte-macrophage colony-stimulating factor, by CD4+ T cells is a key process for amplifying immune responses but can also lead to harmful tissue damage in pathologies like multiple sclerosis and Covid-19. Correctly controlling the expression of proinflammatory cytokines is therefore of major interest. However, the pathogenic signature of CD4+ T cells relies on a transcriptional program that is thus far poorly understood. Here, we identified the transcription factor Ikaros as an essential transcriptional repressor of proinflammatory cytokine gene expression. Our work identifies a critical molecular pathway regulating the pathogenic program of CD4+ T cells and brings new perspectives for potential therapies of autoimmune and inflammatory diseases.
Microarray data sets are accessible in the Gene Expression Omnibus data bank with the accession number [GSE133878][1]. The ChIP-seq, ATAC-seq, and RNA-seq data accession number is [GSE157813][2]. All other study data are included in the article and/or supporting information.
[1]: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE133878
[2]: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE157813