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

GSE272722 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2024/09/29 Platform GPL17021
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE272722_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1138423 and SRA study SRP521210. Searching any of these in the dataset finder brings you back here.

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