IL-31: A new link between T cells and pruritus in atopic skin inflammation
IL-31 is a novel T-cell–derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor. To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases....
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| Published in | Journal of Allergy and Clinical Immunology Vol. 117; no. 2; pp. 411 - 417 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.02.2006
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1097-6825 1365-2567 |
| DOI | 10.1016/j.jaci.2005.10.033 |
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| Abstract | IL-31 is a novel T-cell–derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor.
To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases.
The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis.
IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation.
In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals.
In vitro, staphylococcal enterotoxin B but not viruses or T
H1 and T
H2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside.
Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. |
|---|---|
| AbstractList | IL-31 is a novel T-cell–derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor.
To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases.
The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis.
IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation.
In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals.
In vitro, staphylococcal enterotoxin B but not viruses or T
H1 and T
H2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside.
Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor. Objective To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases. Methods The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis. Results IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T sub(H)1 and T sub(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside. Conclusion Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor. To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases. The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis. IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T(H)1 and T(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside. Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor.BACKGROUNDIL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor.To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases.OBJECTIVETo investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases.The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis.METHODSThe expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis.IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T(H)1 and T(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside.RESULTSIL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T(H)1 and T(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside.Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development.CONCLUSIONOur findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. BACKGROUND: IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor. OBJECTIVE: To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases. METHODS: The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis. RESULTS: IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation. In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In vitro, staphylococcal enterotoxin B but not viruses or T(H)1 and T(H)2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside. CONCLUSION: Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. Background IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of IL-31 receptor A and oncostatin M receptor. Objective To investigate the role of human IL-31 in pruritic and nonpruritic inflammatory skin diseases. Methods The expression of IL-31 was analyzed by quantitative real-time PCR in skin samples of healthy individuals and patients with chronic inflammatory skin diseases. Moreover, IL-31 expression was analyzed in nonlesional skin of atopic dermatitis patients after allergen or superantigen exposure, as well as in stimulated leukocytes. The tissue distribution of the IL-31 receptor heterodimer was investigated by DNA microarray analysis. Results IL-31 was significantly overexpressed in pruritic atopic compared with nonpruritic psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, one of the most pruritic forms of chronic skin inflammation.In vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals.In vitro, staphylococcal enterotoxin B but not viruses or TH1 and TH2 cytokines induced IL-31 in leukocytes. In patients with atopic dermatitis, activated leukocytes expressed significantly higher IL-31 levels compared with control subjects. IL-31 receptor A showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside. Conclusion Our findings provide a new link among staphylococcal colonization, subsequent T-cell recruitment/activation, and pruritus induction in patients with atopic dermatitis. Taken together, these findings show that IL-31 may represent a novel target for antipruritic drug development. |
| Author | Soto, Hortensia Homey, Bernhard Dieu-Nosjean, Marie-Caroline Hoffmann, Thomas K. Muller, Anja Pivarcsi, Andor Rieker, Juliane Lauerma, Antti I. Steinhoff, Martin Alenius, Harri Kemeny, Lajos Meller, Stephan Zlotnik, Albert Sonkoly, Eniko Ruzicka, Thomas |
| Author_xml | – sequence: 1 givenname: Eniko surname: Sonkoly fullname: Sonkoly, Eniko organization: From the Department of Dermatology – sequence: 2 givenname: Anja surname: Muller fullname: Muller, Anja organization: Department of Radiation Oncology – sequence: 3 givenname: Antti I. surname: Lauerma fullname: Lauerma, Antti I. organization: Finnish Institute of Occupational Health, Section of Dermatology, and Skin and Allergy Hospital, Helsinki University Central Hospital – sequence: 4 givenname: Andor surname: Pivarcsi fullname: Pivarcsi, Andor organization: From the Department of Dermatology – sequence: 5 givenname: Hortensia surname: Soto fullname: Soto, Hortensia organization: Neurocrine Biosciences Inc, San Diego – sequence: 6 givenname: Lajos surname: Kemeny fullname: Kemeny, Lajos organization: Department of Dermatology and Allergology, University of Szeged – sequence: 7 givenname: Harri surname: Alenius fullname: Alenius, Harri organization: Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health – sequence: 8 givenname: Marie-Caroline surname: Dieu-Nosjean fullname: Dieu-Nosjean, Marie-Caroline organization: Institut National de la Santé et de la Recherche Médicale U255, Laboratoire d'Immunologie Cellulaire et Clinique, Centre de Recherches Biomedicales des Cordeliers, Paris – sequence: 9 givenname: Stephan surname: Meller fullname: Meller, Stephan organization: From the Department of Dermatology – sequence: 10 givenname: Juliane surname: Rieker fullname: Rieker, Juliane organization: From the Department of Dermatology – sequence: 11 givenname: Martin surname: Steinhoff fullname: Steinhoff, Martin organization: Department of Dermatology, University Hospital of Münster – sequence: 12 givenname: Thomas K. surname: Hoffmann fullname: Hoffmann, Thomas K. organization: Department of Otorhinolaryngology, Heinrich-Heine-University, Düsseldorf – sequence: 13 givenname: Thomas surname: Ruzicka fullname: Ruzicka, Thomas organization: From the Department of Dermatology – sequence: 14 givenname: Albert surname: Zlotnik fullname: Zlotnik, Albert organization: Neurocrine Biosciences Inc, San Diego – sequence: 15 givenname: Bernhard surname: Homey fullname: Homey, Bernhard email: Bernhard.Homey@uni-duesseldorf.de organization: From the Department of Dermatology |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17508384$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/16461142$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-421707$$DView record from Swedish Publication Index |
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| Keywords | pruritus SEB atopic dermatitis cytokines TSST-1 T cells superantigen OSMR IL-31RA IL-31 Allergy Immunopathology Skin disease Cytokine Inflammation Pruritus Atopy Immunology Atopic dermatitis Interleukin 31 T-Lymphocyte Superantigen |
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| Snippet | IL-31 is a novel T-cell–derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed... IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed... Background IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric... BACKGROUND: IL-31 is a novel T-cell-derived cytokine that induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric... |
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| SubjectTerms | Allergic diseases Allergies atopic dermatitis Biological and medical sciences Cell culture Chemokines Cytokines Dermatitis Dermatitis, Atopic - immunology Dermatitis, Atopic - metabolism Dermatitis, Atopic - physiopathology Fundamental and applied biological sciences. Psychology Fundamental immunology Ganglia, Spinal - metabolism Gene expression Humans IL-31 Immunopathology Interleukins - metabolism Ligands Lymphocyte Activation Lymphocytes Medical sciences Prurigo - immunology Prurigo - metabolism pruritus Pruritus - immunology Pruritus - metabolism Pruritus - physiopathology Psoriasis Psoriasis - immunology Psoriasis - metabolism Quality of life Receptors, Interleukin - metabolism Rodents Skin Skin allergic diseases. Stinging insect allergies Staphylococcus aureus - immunology Statistical analysis Studies superantigen Superantigens - immunology T cells T-Lymphocytes - immunology Up-Regulation |
| Title | IL-31: A new link between T cells and pruritus in atopic skin inflammation |
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