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Effect of LAIR-1 deficiency on naïve CD8 T cells at baseline

ABSTRACT: To determine intrinsic differences after genetic ablation of LAIR-1 in naïve CD8 T cells, isolated cells were transcriptionally profiled

ORGANISM(S): Mus musculus

PROVIDER: GSE228710 | GEO | 2025/04/01

REPOSITORIES: GEO

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Effect of LAIR-1 deficiency on naïve CD8 T cells at baseline

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RNA sequencing (RNA-seq) of LAIR-1 overexpression in SKOV-3 ovarian cancer cell lines

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Next Generation Sequencing Facilitates Quantitative Analysis of the implication of LAIR-1 in sorted lung macrophage Transcriptomes

Project description:Recent studies reported the inhibitory properties of LAIR-1 in different inflammatory diseases, including allergic and viral airway inflammation. However, the implication of LAIR-1 in ALI/ARDS remains unknown. Poly(I:C), a synthetic analog of (ds)RNA was administrated intranasally to mimic acute inflammation in viral infections and therefore induce experimental ALI/ARDS. RNA sequencing approach was used to explore and compare lung macrophage transcriptomic profiles in wild-type and LAIR-1 knock-out mice.

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Next Generation Sequencing Facilitates Quantitative Analysis of the implication of LAIR-1 in sorted mouse pulmonary ILC2 Transcriptomes

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Project description:Defining how human pluripotent cell identity is controlled and in particular how naïve pluripotency is acquired during cell reprogramming is crucial for the future applications of pluripotent stem cells. However, the regulatory pathways of naïve cell reprogramming remain incompletely understood. Here, we used genome-wide CRISPR-Cas9 screening to identify novel regulators of primed to naïve pluripotent stem cell reprogramming, including genes that are essential for reprogramming and genes that normally impede reprogramming and whose targeted deletion led to enhanced reprogramming. Integrated analysis defined specific chromatin complexes and signalling pathways as critical regulators of naïve reprogramming, and were largely distinct from regulators of somatic cell reprogramming. Mechanistically, PRC1.3 and PRDM14 are jointly required to transcriptionally repress developmental and gene regulatory factors to ensure naïve cell reprogramming. Additionally, small molecule inhibitors of reprogramming impediments increased the efficiency of naïve cell reprogramming, and are of practical benefit that can improve on current reprogramming methods. Taken together, we have identified novel regulators controlling the establishment of naïve pluripotency in human cells, which will open up new ways to exploit the full potential of pluripotent stem cells. These results also provide new insights into mechanisms that destabilise and reconfigure cell identity during cell state transitions.

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