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C-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

ABSTRACT: c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

PROVIDER: PRJNA601925 | ENA |

REPOSITORIES: ENA

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c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells.

Project description: Not available

| S-EPMC7025824 | biostudies-literature

c-Maf restrains T-bet-driven programming of CCR6-negative group 3 innate lymphoid cells

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Project description:To detect the miRNA expression profile in CCR6+ regulatory T cells In this study, the total RNA was extracted from CCR6+ regulatory T cells and CCR6- regulatory T cells. Then, the expression profile of miRNA on these cells was detected by microarray.

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WT vs c-Maf KO fetal liver macrophage

Project description:Homozygous disruption of c-Maf led to embryonic lethality and impaired erythroblastic island formation. c-Maf is expressed in the fetal liver macrophages. It suggests that macrophages are responsible for the lethality of c-Maf knock-out embryos. To search downstream genes of c-Maf, we surveyed genes associated with macrophage function by microarray analysis. keywords: c-Maf, macrophage, erythroblastic islands, WT (c-Maf WT) and c-Maf KO (c-Maf KO) fetal liver macrophages were sorted by a FACSAria cell sorter. Total RNAs from those macrophages were prepared using RNeasy Kit. Genes down-regulated in c-Maf KO macrophages were searched by GeneSpring software.

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Study of the role of c-Maf in type 2 innate lymphoid cells

Project description:Group 2 innate lymphoid cells (ILC2s) are involved in type 2 inflammatory diseases such as allergy. In response to repeated allergen inhalations, lung epithelial cells secrete innate cytokines that activate ILC2s to release interleukin-5 (IL-5) and interleukin-13 (IL-13) resulting in eosinophil infiltration, mucus hyper-production, and airway hyperreactivity. Beside GATA3, very little is known about the role of specific transcription factors in the regulation of ILC2’s function. Here we identify c-Maf as a crucial regulator of ILC2 function and identity. c-Maf deficient ILC2s are impaired in IL-5 and IL-13 production and eosinophil recruitment. Transcriptomic analysis underlined a reduced expression of genes associated with Th2/ILC2 identity and memory development that we confirmed both in mice and human, either in ILC2s engineered to express less c-Maf or in naturally c-Maflow ILC2s from cord blood. Our results indicate that c-Maf is a core node that connects immature to primed/trained ILC2s.

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Molecular mechanisms of HIV-1 permissiveness in CCR4+CCR6+ Th17 cells

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