Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells.

Autor:	Hosokawa H; Division of Biology & Biological Engineering, California Institute of Technology, Pasadena, CA.; Department of Immunology, Tokai University School of Medicine, Isehara, Kanagawa, Japan., Romero-Wolf M; Division of Biology & Biological Engineering, California Institute of Technology, Pasadena, CA., Yang Q; Department of Immunology and Microbial Disease, Albany Medical College, Albany, NY., Motomura Y; Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.; Laboratory for Innate Immune Systems, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka, Japan., Levanon D; Weizmann Institute of Science, Rehovot, Israel., Groner Y; Weizmann Institute of Science, Rehovot, Israel., Moro K; Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.; Laboratory for Innate Immune Systems, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka, Japan., Tanaka T; Department of Molecular Diagnosis, Graduate School of Medicine, Chiba University, Chiba, Japan.; Agency for Medical Research and Development - Core Research for Evolutionary Medical Science and Technology (AMED-CREST), Graduate School of Medicine, Chiba University, Chiba, Japan., Rothenberg EV; Division of Biology & Biological Engineering, California Institute of Technology, Pasadena, CA.
Jazyk:	angličtina
Zdroj:	The Journal of experimental medicine [J Exp Med] 2020 Jan 06; Vol. 217 (1).
DOI:	10.1084/jem.20190972
Abstrakt:	The zinc finger transcription factor, Bcl11b, is expressed in T cells and group 2 innate lymphoid cells (ILC2s) among hematopoietic cells. In early T-lineage cells, Bcl11b directly binds and represses the gene encoding the E protein antagonist, Id2, preventing pro-T cells from adopting innate-like fates. In contrast, ILC2s co-express both Bcl11b and Id2. To address this contradiction, we have directly compared Bcl11b action mechanisms in pro-T cells and ILC2s. We found that Bcl11b binding to regions across the genome shows distinct cell type-specific motif preferences. Bcl11b occupies functionally different sites in lineage-specific patterns and controls totally different sets of target genes in these cell types. In addition, Bcl11b bears cell type-specific post-translational modifications and organizes different cell type-specific protein complexes. However, both cell types use the same distal enhancer region to control timing of Bcl11b activation. Therefore, although pro-T cells and ILC2s both need Bcl11b for optimal development and function, Bcl11b works substantially differently in these two cell types. (© 2019 Hosokawa et al.)
Databáze:	MEDLINE
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