For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
40
views
31
references
 Top references
cited by
172
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      62
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Interleukin 9 fate reporter reveals induction of innate IL-9 response in lung inflammation

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Interleukin 9 (IL-9) is a cytokine implicated in lung inflammation, but its cellular origin and function remain unclear. Here we describe a reporter mouse strain designed to fate map cells that have activated IL-9. We show that during papain-induced lung inflammation IL-9 production was largely restricted to innate lymphoid cells (ILC). IL-9 production by ILC was dependent on IL-2 from adaptive immune cells and was rapidly lost in favor of other cytokines, such as IL-13 and IL-5. Blockade of IL-9 production via neutralizing antibodies substantially reduced IL-13 and IL-5, suggesting that ILC provide the missing link between the well-established functions of IL-9 on the regulation of T H2 cytokines and responses.

          Related collections

          Most cited references31

          • Record: found
          • Abstract: found
          • Article: not found

          IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo.

          Madeline M. Fort, Jeanne Cheung, David H.Y. Yen … (2001)
          We have characterized a cytokine produced by Th2 cells, designated as IL-25. Infusion of mice with IL-25 induced IL-4, IL-5, and IL-13 gene expression. The induction of these cytokines resulted in Th2-like responses marked by increased serum IgE, IgG(1), and IgA levels, blood eosinophilia, and pathological changes in the lungs and digestive tract that included eosinophilic infiltrates, increased mucus production, and epithelial cell hyperplasia/hypertrophy. In addition, our studies show that IL-25 induces Th2-type cytokine production by accessory cells that are MHC class II(high), CD11c(dull), and lineage(-). These results suggest that IL-25, derived from Th2 T cells, is capable of amplifying allergic type inflammatory responses by its actions on other cell types.
          Article 0 comments Cited 341 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset.

            Marc Veldhoen, Catherine Uyttenhove, Jacques Van Snick … (2008)
            Since the discovery of T helper type 1 and type 2 effector T cell subsets 20 years ago, inducible regulatory T cells and interleukin 17 (IL-17)-producing T helper cells have been added to the 'portfolio' of helper T cells. It is unclear how many more effector T cell subsets there may be and to what degree their characteristics are fixed or flexible. Here we show that transforming growth factor-beta, a cytokine at the center of the differentiation of IL-17-producing T helper cells and inducible regulatory T cells, 'reprograms' T helper type 2 cells to lose their characteristic profile and switch to IL-9 secretion or, in combination with IL-4, drives the differentiation of 'T(H)-9' cells directly. Thus, transforming growth factor-beta constitutes a regulatory 'switch' that in combination with other cytokines can 'reprogram' effector T cell differentiation along different pathways.
            Article 0 comments Cited 338 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Identification of an interleukin (IL)-25–dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion

              Padraic Fallon, Sarah Ballantyne, Niamh E Mangan … (2006)
              Type 2 immunity, which involves coordinated regulation of innate and adaptive immune responses, can protect against helminth parasite infection, but may lead to allergy and asthma after inappropriate activation. We demonstrate that il25−/− mice display inefficient Nippostrongylus brasiliensis expulsion and delayed cytokine production by T helper 2 cells. We further establish a key role for interleukin (IL)-25 in regulating a novel population of IL-4–, IL-5–, IL-13–producing non–B/non–T (NBNT), c-kit+, FcɛR1− cells during helminth infection. A deficit in this population in il25−/− mice correlates with inefficient N. brasiliensis expulsion. In contrast, administration of recombinant IL-25 in vivo induces the appearance of NBNT, c-kit+, FcɛR1− cells and leads to rapid worm expulsion that is T and B cell independent, but type 2 cytokine dependent. We demonstrate that these IL-25–regulated cells appear rapidly in the draining lymph nodes, implicating them as a source of type 2 cytokines during initiation of worm expulsion.
              Article 0 comments Cited 260 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-journal-id): 100941354
                Journal ID (pubmed-jr-id): 21750
                Journal ID (nlm-ta): Nat Immunol
                Journal ID (iso-abbrev): Nat. Immunol.
                Title: Nature immunology
                ISSN (Print): 1529-2908
                ISSN (Electronic): 1529-2916
                Publication date Nihms-submitted: 7 September 2011
                Publication date (Electronic): 09 October 2011
                Publication date PMC-release: 01 May 2012
                Volume: 12
                Issue: 11
                Pages: 1071-1077
                Affiliations
                [* ]Division of Molecular Immunology, MRC National Institute for Medical Research, Mill Hill, UK
                [$ ]Division of Molecular Structure, MRC National Institute for Medical Research, Mill Hill, UK
                [§ ]Ludwig Institute for Cancer Research, Brussels, Belgium
                [# ]London School of Hygiene and Tropical Medicine Keppel Street, London, UK
                [& ]Twincore, Institut für Infektionsimmunologie, Hannover, Germany
                Author notes
                [@]

                present address: Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California, USA

                Article
                Manuscript ID: UKMS36406
                DOI: 10.1038/ni.2133
                PMC ID: 3198843
                PubMed ID: 21983833
                SO-VID: 46c5bdbb-8006-49f1-a802-167195e79f31
                License:

                Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms

                History
                Funding
                Funded by: Medical Research Council :
                Award ID: U.1175.02.003.00003(60535) || MRC_
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

                Comments

                Comment on this article

                scite_

                Similar content62

                See all similar

                Cited by169

                See all cited by