| Literature DB >> 31618654 |
Heping Xu1, Jiarui Ding2, Caroline B M Porter2, Antonia Wallrapp3, Marcin Tabaka2, Sai Ma2, Shujie Fu4, Xuanxuan Guo4, Samantha J Riesenfeld2, Chienwen Su5, Danielle Dionne2, Lan T Nguyen2, Ariel Lefkovith2, Orr Ashenberg2, Patrick R Burkett3, Hai Ning Shi5, Orit Rozenblatt-Rosen2, Daniel B Graham6, Vijay K Kuchroo7, Aviv Regev8, Ramnik J Xavier9.
Abstract
Signaling abnormalities in immune responses in the small intestine can trigger chronic type 2 inflammation involving interaction of multiple immune cell types. To systematically characterize this response, we analyzed 58,067 immune cells from the mouse small intestine by single-cell RNA sequencing (scRNA-seq) at steady state and after induction of a type 2 inflammatory reaction to ovalbumin (OVA). Computational analysis revealed broad shifts in both cell-type composition and cell programs in response to the inflammation, especially in group 2 innate lymphoid cells (ILC2s). Inflammation induced the expression of exon 5 of Calca, which encodes the alpha-calcitonin gene-related peptide (α-CGRP), in intestinal KLRG1+ ILC2s. α-CGRP antagonized KLRG1+ ILC2s proliferation but promoted IL-5 expression. Genetic perturbation of α-CGRP increased the proportion of intestinal KLRG1+ ILC2s. Our work highlights a model where α-CGRP-mediated neuronal signaling is critical for suppressing ILC2 expansion and maintaining homeostasis of the type 2 immune machinery.Entities:
Keywords: CGRP; allergic inflammation; batch effect correction; intestinal immune cell atlas; neuro-immune interaction; neuropeptides; scRNA-seq; single cell genomics; topic model; type 2 innate lymphoid cells
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Year: 2019 PMID: 31618654 PMCID: PMC6991097 DOI: 10.1016/j.immuni.2019.09.004
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745