| Literature DB >> 23603794 |
Ben Roediger1, Ryan Kyle, Kwok Ho Yip, Nital Sumaria, Thomas V Guy, Brian S Kim, Andrew J Mitchell, Szun S Tay, Rohit Jain, Elizabeth Forbes-Blom, Xi Chen, Philip L Tong, Holly A Bolton, David Artis, William E Paul, Barbara Fazekas de St Groth, Michele A Grimbaldeston, Graham Le Gros, Wolfgang Weninger.
Abstract
Type 2 immunity is critical for defense against cutaneous infections but also underlies the development of allergic skin diseases. We report the identification in normal mouse dermis of an abundant, phenotypically unique group 2 innate lymphoid cell (ILC2) subset that depended on interleukin 7 (IL-7) and constitutively produced IL-13. Intravital multiphoton microscopy showed that dermal ILC2 cells specifically interacted with mast cells, whose function was suppressed by IL-13. Treatment of mice deficient in recombination-activating gene 1 (Rag1(-/-)) with IL-2 resulted in the population expansion of activated, IL-5-producing dermal ILC2 cells, which led to spontaneous dermatitis characterized by eosinophil infiltrates and activated mast cells. Our data show that ILC2 cells have both pro- and anti-inflammatory properties and identify a previously unknown interactive pathway between two innate populations of cells of the immune system linked to type 2 immunity and allergic diseases.Entities:
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Year: 2013 PMID: 23603794 PMCID: PMC4282745 DOI: 10.1038/ni.2584
Source DB: PubMed Journal: Nat Immunol ISSN: 1529-2908 Impact factor: 25.606