Hans Jürgen Hoffmann

Increased IL-17RA and IL-17RC in End-Stage COPD and the Contribution to Mast Cell Secretion of FGF-2 and VEGF

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  • Abraham B Roos, AstraZeneca R&D Gothenburg, Respiratory, Inflammation and Autoimmunity, Innovative Medicines, Pepparedsleden 1, 431 83, Mölndal, Sweden. abraham.roos@astrazeneca.com.
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  • Michiko Mori, Department of Experimental Medical Science, Lund University, Lund, Sweden.
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  • Harpreet K Gura, Institute of Clinical Medicine, Aarhus University, and Department of Respiratory Diseases and Allergy B, Aarhus University Hospital, Aarhus, Denmark.
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  • Axel Lorentz, Department of Nutritional Medicine, University of Hohenheim, Stuttgart, Germany.
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  • Leif Bjermer, Department of Respiratory Medicine and Allergology, Lund University, Lund, Sweden.
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  • Hans Jürgen Hoffmann
  • Jonas S Erjefält, Department of Experimental Medical Science, Lund University, Lund, Sweden.
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  • Martin R Stampfli, Department of Medicine, Firestone Institute of Respiratory Health at St. Joseph's Health Care, Hamilton, ON, Canada.

Mast cells are accumulated in advanced chronic obstructive pulmonary disease (COPD), and interleukin (IL)-17 signaling plays a role in disease progression. The expression, localization and functional relevance of IL-17 receptor (R)A and IL-17RC was explored in COPD by immunodetection, and functional assays.IL-17RA and IL-17RC was increased in very severe COPD, and expressed by mast cells. Increased secretion of the pro-angiogenic basic fibroblast growth factor and vascular endothelial growth factor was observed in vitro-maintained mast cells stimulated with IL-17A. Expression of these mediators was confirmed in end-stage COPD. Thus, accumulation of mast cells in COPD may contribute to vascular remodeling.

Original languageEnglish
Article number48
JournalRespiratory Medicine
Number of pages4
Publication statusPublished - 15 Mar 2017

    Research areas

  • Letter

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