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Transcriptional Atlas of Intestinal Immune Cells Reveals that Neuropeptide α-CGRP Modulates Group 2 Innate Lymphoid Cell Responses.
Xu, Heping; Ding, Jiarui; Porter, Caroline B M; Wallrapp, Antonia; Tabaka, Marcin; Ma, Sai; Fu, Shujie; Guo, Xuanxuan; Riesenfeld, Samantha J; Su, Chienwen; Dionne, Danielle; Nguyen, Lan T; Lefkovith, Ariel; Ashenberg, Orr; Burkett, Patrick R; Shi, Hai Ning; Rozenblatt-Rosen, Orit; Graham, Daniel B; Kuchroo, Vijay K; Regev, Aviv; Xavier, Ramnik J.
Afiliación
  • Xu H; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Key Laboratory of Structural Biology of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou 310024, Zhejiang Province, China; Laboratory of Systems Immunology, Institute of Basic Medical Sciences, Westlake Institute
  • Ding J; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Porter CBM; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Wallrapp A; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02114, USA.
  • Tabaka M; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Ma S; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Fu S; Key Laboratory of Structural Biology of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou 310024, Zhejiang Province, China; Laboratory of Systems Immunology, Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou 310024, Zhejiang Province, China.
  • Guo X; Key Laboratory of Structural Biology of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou 310024, Zhejiang Province, China; Laboratory of Systems Immunology, Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Hangzhou 310024, Zhejiang Province, China.
  • Riesenfeld SJ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Su C; Mucosal Immunology and Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
  • Dionne D; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Nguyen LT; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Lefkovith A; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Ashenberg O; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Burkett PR; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02114, USA.
  • Shi HN; Mucosal Immunology and Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
  • Rozenblatt-Rosen O; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
  • Graham DB; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Harvard Medical
  • Kuchroo VK; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02114, USA.
  • Regev A; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Howard Hughes Medical Institute and Koch Institute for Integrative Cancer Research, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA. Electronic address: aregev@broadinstitute.org.
  • Xavier RJ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Molecular Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA; Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Harvard Medical
Immunity ; 51(4): 696-708.e9, 2019 10 15.
Article en En | MEDLINE | ID: mdl-31618654
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.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neuropéptidos / Linfocitos / Péptido Relacionado con Gen de Calcitonina / Inflamación / Intestinos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Immunity Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2019 Tipo del documento: Article
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Neuropéptidos / Linfocitos / Péptido Relacionado con Gen de Calcitonina / Inflamación / Intestinos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Immunity Asunto de la revista: ALERGIA E IMUNOLOGIA Año: 2019 Tipo del documento: Article