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PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [scRNA-seq]

ABSTRACT: PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [scRNA-seq]

PROVIDER: PRJNA1138424 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29907601.fastq.gz	Fastqsanger.gz
	SRR29907602.fastq.gz	Fastqsanger.gz
	SRR29907603.fastq.gz	Fastqsanger.gz
	SRR29907604.fastq.gz	Fastqsanger.gz
	SRR29907605.fastq.gz	Fastqsanger.gz

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PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [scRNA-seq]

Project description:Dysfunction of group II innate lymphoid cells (ILC2s) plays an important role in the development of type II inflammation-related diseases such as asthma and pulmonary fibrosis. Notably, neural signals are increasingly recognized as pivotal regulators of ILC2s. However, how ILC2s intrinsically modulate their responsiveness to these neural signals is still largely unknown. Here, using single-cell RNA sequencing and bulk mRNA sequencing, we report that the immune regulatory molecule PAC1 (phosphatase of activated cells 1) selectively promotes the signaling of neuropeptide CGRP (calcitonin gene-related peptide) in ILC2s. Moreover, PAC1 is necessary for ensuring the expression of CGRP-response genes by influencing chromatin accessibility. In summary, our study demonstrates that PAC1 is an important regulator of ILC2 responses and we propose that PAC1 is a potential target for therapeutic interventions of type II inflammation-related diseases.

2024-09-29 | GSE272724 | GEO

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [RNA-seq]

2024-09-29 | GSE272723 | GEO

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [FastATAC-seq]

2024-09-29 | GSE272722 | GEO

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [RNA-seq]

Project description:PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [RNA-seq]

| PRJNA1138422 | ENA

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [FastATAC-seq]

Project description:PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [FastATAC-seq]

| PRJNA1138423 | ENA

PAC1 constrains type 2 inflammation through promotion of CGRP signaling in ILC2s.

Project description:Dysfunction of group 2 innate lymphoid cells (ILC2s) plays an important role in the development of type 2 inflammation-related diseases such as asthma and pulmonary fibrosis. Notably, neural signals are increasingly recognized as pivotal regulators of ILC2s. However, how ILC2s intrinsically modulate their responsiveness to these neural signals is still largely unknown. Here, using single-cell RNA-Seq, we found that the immune-regulatory molecule phosphatase of activated cells 1 (PAC1) selectively promoted the signaling of the neuropeptide calcitonin gene-related peptide (CGRP) in ILC2s in a cell-intrinsic manner. Genetic ablation of PAC1 in ILC2s substantially impaired the inhibitory effect of CGRP on proliferation and IL-13 secretion. PAC1 deficiency significantly exacerbated allergic airway inflammation induced by Alternaria alternata or papain in mice. Moreover, in human circulating ILC2s, the expression level of PAC1 was also significantly negatively correlated with the number of ILC2s and their expression level of IL13. Mechanistically, PAC1 was necessary for ensuring the expression of CGRP response genes by influencing chromatin accessibility. In summary, our study demonstrated that PAC1 is an important regulator of ILC2 responses, and we propose that PAC1 is a potential target for therapeutic interventions in type 2 inflammation-related diseases.

| S-EPMC11527444 | biostudies-literature

Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation

Project description:Innate and adaptive lymphocytes work in concert to maintain tissue homeostasis and to mediate host defense at mucosal barriers. Herein, we used single cell analysis to show substantial diversity of gene expression in ILCs and T helper cells during a helminth infection in the lung. Notably, we found that the Calca gene, which is spliced to generate the neuropeptide CGRP, was selectively transcribed in ILC2s and Th2 cells in an activation dependent manner. The Calca locus acquired chromatin accessibility at the ILC2 precursor stage and is pre-programmed for rapid production of CGRP upon ILC2 activation. CGRP globally antagonized actions of neuromedin U (NMU) and the alarmin IL-33. However, CGRP selectively acted in concert with NMU and IL-33 to promote IL-5 expression, but not IL-13. The complex interplay among neuropeptides and alarmin fine-tunes type 2 immune responses and will undoubtedly become more relevant as therapeutic neuropeptide blockade advances in the clinic.

2019-06-25 | GSE131996 | GEO

Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation

Project description:Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation

| PRJNA545529 | ENA

Pac1+/+ versus Pac1-/- TG-macrophages_LPS 6h

Project description:LPS-stimulated macrophages from Pac1+/+ and Pac1-/- mice were compared to assess gene expression changes in the absence of PAC-1 (also known as Dual specificity phosphatase 2). Keywords: Comparison of Pac1+/+ with Pac1-/- activated macrophages

2006-01-10 | GSE3993 | GEO

Transcription profiling of mouse macrophaes and mast cells from Pac1+/+ versus Pac1-/- animals

Project description:This SuperSeries is composed of the following subset Series:; GSE3993: Pac1+/+ versus Pac1-/- TG-macrophages_LPS 6h; GSE3994: Pac1+/+ versus Pac1-/- BMMCs_IgE-DNP 2 h Experiment Overall Design: Refer to individual Series

2008-06-12 | E-GEOD-4014 | biostudies-arrayexpress

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