IL-25/IL-33–responsive TH2 cells characterize nasal polyps with a default TH17 signature in nasal mucosa
Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosa...
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| Published in | Journal of allergy and clinical immunology Vol. 137; no. 5; pp. 1514 - 1524 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.05.2016
Elsevier Limited Mosby |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1097-6825 |
| DOI | 10.1016/j.jaci.2015.10.019 |
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| Abstract | Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosal T-cell responses is unknown.
We sought to investigate the role of the IL-25/IL-33 axis in local mucosal T-cell responses in patients with CRSwNP.
Polyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsy specimens and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T-cell surface phenotype/intracellular cytokines were assessed by means of flow cytometry. T-cell receptor variable β-chain analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis.
IL-25 receptor (IL-17RB)–expressing TH2 effector cells were identified in nasal polyp tissue but not the healthy nasal mucosa or periphery. IL-17RB+CD4+ polyp–derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB+CD4+ T cells, several identical T-cell receptor variable β-chain complementarity-determining region 3 sequences were identified in different subjects, suggesting clonal expansion driven by a common antigen. Abundant IL-17–producing T cells were observed in both healthy nasal mucosal and polyp populations, with TH17-related genes the most overexpressed compared with peripheral blood T cells.
IL-25 and IL-33 can interact locally with IL-17RB+ST2+ polyp T cells to augment TH2 responses in patients with CRSwNP. A local TH17 response might be important in healthy nasal mucosal immune homeostasis. |
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| AbstractList | Background Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosal T-cell responses is unknown. Objective We sought to investigate the role of the IL-25/IL-33 axis in local mucosal T-cell responses in patients with CRSwNP. Methods Polyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsy specimens and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T-cell surface phenotype/intracellular cytokines were assessed by means of flow cytometry. T-cell receptor variable β-chain analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis. Results IL-25 receptor (IL-17RB)-expressing TH2 effector cells were identified in nasal polyp tissue but not the healthy nasal mucosa or periphery. IL-17RB+CD4+polyp-derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB+CD4+T cells, several identical T-cell receptor variable β-chain complementarity-determining region 3 sequences were identified in different subjects, suggesting clonal expansion driven by a common antigen. Abundant IL-17-producing T cells were observed in both healthy nasal mucosal and polyp populations, with TH17-related genes the most overexpressed compared with peripheral blood T cells. Conclusion IL-25 and IL-33 can interact locally with IL-17RB+ST2+polyp T cells to augment TH2 responses in patients with CRSwNP. A local TH17 response might be important in healthy nasal mucosal immune homeostasis. Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosal T-cell responses is unknown. We sought to investigate the role of the IL-25/IL-33 axis in local mucosal T-cell responses in patients with CRSwNP. Polyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsy specimens and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T-cell surface phenotype/intracellular cytokines were assessed by means of flow cytometry. T-cell receptor variable β-chain analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis. IL-25 receptor (IL-17RB)–expressing TH2 effector cells were identified in nasal polyp tissue but not the healthy nasal mucosa or periphery. IL-17RB+CD4+ polyp–derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB+CD4+ T cells, several identical T-cell receptor variable β-chain complementarity-determining region 3 sequences were identified in different subjects, suggesting clonal expansion driven by a common antigen. Abundant IL-17–producing T cells were observed in both healthy nasal mucosal and polyp populations, with TH17-related genes the most overexpressed compared with peripheral blood T cells. IL-25 and IL-33 can interact locally with IL-17RB+ST2+ polyp T cells to augment TH2 responses in patients with CRSwNP. A local TH17 response might be important in healthy nasal mucosal immune homeostasis. Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosal T-cell responses is unknown.BACKGROUNDChronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosal T-cell responses is unknown.We sought to investigate the role of the IL-25/IL-33 axis in local mucosal T-cell responses in patients with CRSwNP.OBJECTIVEWe sought to investigate the role of the IL-25/IL-33 axis in local mucosal T-cell responses in patients with CRSwNP.Polyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsy specimens and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T-cell surface phenotype/intracellular cytokines were assessed by means of flow cytometry. T-cell receptor variable β-chain analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis.METHODSPolyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsy specimens and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T-cell surface phenotype/intracellular cytokines were assessed by means of flow cytometry. T-cell receptor variable β-chain analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis.IL-25 receptor (IL-17RB)-expressing TH2 effector cells were identified in nasal polyp tissue but not the healthy nasal mucosa or periphery. IL-17RB(+)CD4(+) polyp-derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB(+)CD4(+) T cells, several identical T-cell receptor variable β-chain complementarity-determining region 3 sequences were identified in different subjects, suggesting clonal expansion driven by a common antigen. Abundant IL-17-producing T cells were observed in both healthy nasal mucosal and polyp populations, with TH17-related genes the most overexpressed compared with peripheral blood T cells.RESULTSIL-25 receptor (IL-17RB)-expressing TH2 effector cells were identified in nasal polyp tissue but not the healthy nasal mucosa or periphery. IL-17RB(+)CD4(+) polyp-derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB(+)CD4(+) T cells, several identical T-cell receptor variable β-chain complementarity-determining region 3 sequences were identified in different subjects, suggesting clonal expansion driven by a common antigen. Abundant IL-17-producing T cells were observed in both healthy nasal mucosal and polyp populations, with TH17-related genes the most overexpressed compared with peripheral blood T cells.IL-25 and IL-33 can interact locally with IL-17RB(+)ST2(+) polyp T cells to augment TH2 responses in patients with CRSwNP. A local TH17 response might be important in healthy nasal mucosal immune homeostasis.CONCLUSIONIL-25 and IL-33 can interact locally with IL-17RB(+)ST2(+) polyp T cells to augment TH2 responses in patients with CRSwNP. A local TH17 response might be important in healthy nasal mucosal immune homeostasis. Background Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2 innate lymphoid cells from polyps produce IL-5 and IL-13 in response to IL-25 and IL-33, although the relevance of this axis to local mucosal T-cell responses is unknown. Objective We sought to investigate the role of the IL-25/IL-33 axis in local mucosal T-cell responses in patients with CRSwNP. Methods Polyp tissue and blood were obtained from patients undergoing nasal polypectomy. Control nasal biopsy specimens and blood were obtained from healthy volunteers. Tissue was cultured in a short-term explant model. T-cell surface phenotype/intracellular cytokines were assessed by means of flow cytometry. T-cell receptor variable beta -chain analysis was performed with the immunoSEQ assay. Microarrays were performed for gene expression analysis. Results IL-25 receptor (IL-17RB)-expressing TH2 effector cells were identified in nasal polyp tissue but not the healthy nasal mucosa or periphery. IL-17RB+CD4+ polyp-derived TH2 cells coexpressed ST2 (IL-33 receptor) and responded to IL-25 and IL-33 with enhanced IL-5 and IL-13 production. Within IL-17RB+CD4+ T cells, several identical T-cell receptor variable beta -chain complementarity-determining region 3 sequences were identified in different subjects, suggesting clonal expansion driven by a common antigen. Abundant IL-17-producing T cells were observed in both healthy nasal mucosal and polyp populations, with TH17-related genes the most overexpressed compared with peripheral blood T cells. Conclusion IL-25 and IL-33 can interact locally with IL-17RB+ST2+ polyp T cells to augment TH2 responses in patients with CRSwNP. A local TH17 response might be important in healthy nasal mucosal immune homeostasis. |
| Author | Kariyawasam, Harsha H. Till, Stephen J. Rimmer, Joanne Rana, Batika M.J. Lund, Valerie J. McKenzie, Andrew N.J. Lam, Emily P.S. Powell, Nicholas Orban, Nara Lennartz-Walker, Melissa Durham, Stephen R. Hopkins, Claire Ying, Sun Cousins, David J. |
| AuthorAffiliation | e Division of Transplantation Immunology and Mucosal Biology and Medical Research Council Centre for Transplantation, King's College London, London, United Kingdom b Allergy and Medical Rhinology Section, Royal National Throat Nose Ear Hospital, University College London, London, United Kingdom a Division of Asthma, Allergy and Lung Biology, Guy's Hospital, King's College London, London, United Kingdom c Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom g Department of ENT, Guy's and St Thomas' Hospital, London, United Kingdom h Medical Research Council and Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom f Department of Infection, Immunity and Inflammation, NIHR Leicester Respiratory Biomedical Research Unit, Leicester Institute for Lung Health, University of Leicester, Leicester, United Kingdom d Section of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College London, London, United Kingdom |
| AuthorAffiliation_xml | – name: c Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom – name: b Allergy and Medical Rhinology Section, Royal National Throat Nose Ear Hospital, University College London, London, United Kingdom – name: e Division of Transplantation Immunology and Mucosal Biology and Medical Research Council Centre for Transplantation, King's College London, London, United Kingdom – name: g Department of ENT, Guy's and St Thomas' Hospital, London, United Kingdom – name: a Division of Asthma, Allergy and Lung Biology, Guy's Hospital, King's College London, London, United Kingdom – name: d Section of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College London, London, United Kingdom – name: f Department of Infection, Immunity and Inflammation, NIHR Leicester Respiratory Biomedical Research Unit, Leicester Institute for Lung Health, University of Leicester, Leicester, United Kingdom – name: h Medical Research Council and Asthma UK Centre in Allergic Mechanisms of Asthma, London, United Kingdom |
| Author_xml | – sequence: 1 givenname: Emily P.S. surname: Lam fullname: Lam, Emily P.S. organization: Division of Asthma, Allergy and Lung Biology, Guy's Hospital, King's College London, London, United Kingdom – sequence: 2 givenname: Harsha H. surname: Kariyawasam fullname: Kariyawasam, Harsha H. organization: Allergy and Medical Rhinology Section, Royal National Throat Nose Ear Hospital, University College London, London, United Kingdom – sequence: 3 givenname: Batika M.J. surname: Rana fullname: Rana, Batika M.J. organization: Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom – sequence: 4 givenname: Stephen R. surname: Durham fullname: Durham, Stephen R. organization: Section of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 5 givenname: Andrew N.J. surname: McKenzie fullname: McKenzie, Andrew N.J. organization: Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom – sequence: 6 givenname: Nicholas surname: Powell fullname: Powell, Nicholas organization: Division of Transplantation Immunology and Mucosal Biology and Medical Research Council Centre for Transplantation, King's College London, London, United Kingdom – sequence: 7 givenname: Nara orcidid: 0000-0002-2169-9231 surname: Orban fullname: Orban, Nara organization: Section of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College London, London, United Kingdom – sequence: 8 givenname: Melissa surname: Lennartz-Walker fullname: Lennartz-Walker, Melissa organization: Division of Asthma, Allergy and Lung Biology, Guy's Hospital, King's College London, London, United Kingdom – sequence: 9 givenname: Claire surname: Hopkins fullname: Hopkins, Claire organization: Department of ENT, Guy's and St Thomas' Hospital, London, United Kingdom – sequence: 10 givenname: Sun surname: Ying fullname: Ying, Sun organization: Division of Asthma, Allergy and Lung Biology, Guy's Hospital, King's College London, London, United Kingdom – sequence: 11 givenname: Joanne surname: Rimmer fullname: Rimmer, Joanne organization: Allergy and Medical Rhinology Section, Royal National Throat Nose Ear Hospital, University College London, London, United Kingdom – sequence: 12 givenname: Valerie J. surname: Lund fullname: Lund, Valerie J. organization: Allergy and Medical Rhinology Section, Royal National Throat Nose Ear Hospital, University College London, London, United Kingdom – sequence: 13 givenname: David J. surname: Cousins fullname: Cousins, David J. organization: Department of Infection, Immunity and Inflammation, NIHR Leicester Respiratory Biomedical Research Unit, Leicester Institute for Lung Health, University of Leicester, Leicester, United Kingdom – sequence: 14 givenname: Stephen J. surname: Till fullname: Till, Stephen J. email: stephen.till@kcl.ac.uk organization: Division of Asthma, Allergy and Lung Biology, Guy's Hospital, King's College London, London, United Kingdom |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26684290$$D View this record in MEDLINE/PubMed |
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| Keywords | IL-17RB IL-25 CRSwNP T-cell phenotype IL-33 T-cell receptor Vβ repertoire ST2 ILC2 TH2 cells microarray AIM2 Chronic rhinosinusitis with nasal polyps TCR Vβ nasal mucosa TH17 cells CRTH2 CDR3 T(H)17 cells T(H)2 cells |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These authors contributed equally to this work. |
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| OpenAccessLink | https://www.sciencedirect.com/science/article/pii/S0091674915015730 |
| PMID | 26684290 |
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| PublicationDate | May 2016 2016-05-00 20160501 |
| PublicationDateYYYYMMDD | 2016-05-01 |
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| PublicationDecade | 2010 |
| PublicationPlace | United States |
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| PublicationTitle | Journal of allergy and clinical immunology |
| PublicationTitleAlternate | J Allergy Clin Immunol |
| PublicationYear | 2016 |
| Publisher | Elsevier Inc Elsevier Limited Mosby |
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| Snippet | Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine expression. Type 2... Background Chronic rhinosinusitis with nasal polyposis (CRSwNP) in Western countries is characterized by eosinophilia, IgE production, and TH2 cytokine... |
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| SubjectTerms | Cell culture Chronic Disease Chronic rhinosinusitis with nasal polyps Cloning Cytokines Eosinophilia - immunology Gene expression Genotype & phenotype Humans IL-17RB IL-25 IL-33 Interleukin-17 - immunology Interleukin-33 - immunology Lymphocytes Mechanisms of Allergy and Clinical Immunology microarray nasal mucosa Nasal Mucosa - immunology Nasal Polyps - immunology Rhinitis - immunology Sinusitis - immunology ST2 Studies T cell receptors T-cell phenotype T-cell receptor Vβ repertoire Th17 Cells - immunology TH17 cells TH2 cells Th2 Cells - immunology |
| Title | IL-25/IL-33–responsive TH2 cells characterize nasal polyps with a default TH17 signature in nasal mucosa |
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