Radiosensitive Hematopoietic Cells Determine the Extent of Skin Inflammation in Experimental Epidermolysis Bullosa Acquisita

DOI PDF PubMed 被引用文献2件 オープンアクセス
  • Hiroaki Iwata
    Department of Dermatology, University of Lübeck , D-23538 Lübeck ,
  • Mareike Witte
    Lübeck Institute of Experimental Dermatology, University of Lübeck , D-23538 Lübeck ,
  • Unni Krishna S R L Samavedam
    Lübeck Institute of Experimental Dermatology, University of Lübeck , D-23538 Lübeck ,
  • Yask Gupta
    Lübeck Institute of Experimental Dermatology, University of Lübeck , D-23538 Lübeck ,
  • Atsushi Shimizu
    First Department of Dermatology, School of Medicine, Faculty of Medicine Toho University , Tokyo 143-8540 ,
  • Akira Ishiko
    First Department of Dermatology, School of Medicine, Faculty of Medicine Toho University , Tokyo 143-8540 ,
  • Tobias Schröder
    Lübeck Institute of Experimental Dermatology, University of Lübeck , D-23538 Lübeck ,
  • Karsten Seeger
    Department of Chemistry, University of Lübeck , D-23538 Lübeck ,
  • Markus Dahlke
    Department of Radiation Oncology, University of Lübeck , D-23538 Lübeck ,
  • Dirk Rades
    Department of Radiation Oncology, University of Lübeck , D-23538 Lübeck ,
  • Detlef Zillikens
    Department of Dermatology, University of Lübeck , D-23538 Lübeck ,
  • Ralf J Ludwig
    Department of Dermatology, University of Lübeck , D-23538 Lübeck ,

書誌事項

公開日
2015-09-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.1501003
公開者
Oxford University Press (OUP)

この論文をさがす

説明

<jats:title>Abstract</jats:title> <jats:p>Animal models have enhanced our understanding of the pathogenesis of autoimmune diseases. For these models, genetically identical, inbred mice have commonly been used. Different inbred mouse strains, however, show a high variability in disease manifestation. Identifying the factors that influence this disease variability could provide unrecognized insights into pathogenesis. We established a novel Ab transfer-induced model of epidermolysis bullosa acquisita (EBA), an autoimmune disease characterized by (muco)-cutaneous blistering caused by anti-type VII collagen (COL7) autoantibodies. Blistering after anti-COL7 IgG (directed against the von Willebrand factor A–like domain 2) transfer showed clear variability among inbred mouse strains, that is, severe cutaneous blistering and inflammation in C57BL/6J and absence of skin lesions in MRL/MpJ mice. The transfer of anti-COL7 IgG into irradiated, EBA-resistant MRL/MpJ mice, rescued by transplantation with bone marrow from EBA-susceptible B6.AK-H2k mice, induced blistering. To the contrary, irradiated EBA-susceptible B6.AK-H2k mice that were rescued using MRL/MpJ bone marrow were devoid of blistering. In vitro, immune complex activation of neutrophils from C57BL/6J or MRL/MpJ mice showed an impaired reactive oxygen species release from the latter, whereas no differences were observed after PMA activation. This finding was paralleled by divergent expression profiles of immune complex–activated neutrophils from either C57BL/6J or MRL/MpJ mice. Collectively, we demonstrate that radiosensitive cells determine the varying extent of skin inflammation and blistering in the end-stage effector phase of EBA.</jats:p>

収録刊行物

被引用文献 (2)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ