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Evidence for a contributory role of a xenogeneic immune response in experimental epidermolysis bullosa acquisita
Author(s) -
Niebuhr Markus,
Kasperkiewicz Michael,
Maass Sebastian,
Hauenschild Eva,
Bieber Katja,
Ludwig Ralf J.,
Westermann Jürgen,
Kalies Kathrin
Publication year - 2017
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13439
Subject(s) - epidermolysis bullosa acquisita , immune system , immunology , autoantibody , antibody , epidermolysis bullosa , population , inflammation , biology , autoimmunity , lymph , medicine , pathology , environmental health
Autoimmune diseases affect a large fraction of the population in Western countries. To elucidate the underlying causes, autoantibody transfer‐induced mouse models have been established that greatly contributed to the understanding of the pathophysiology of these diseases. However, the role of a potentially co‐occurring murine xenogeneic immune response to commonly utilized rabbit anti‐mouse IgG remains poorly understood. Using the established rabbit anti‐mouse type VII collagen ( COL 7) IgG‐induced mouse model of the mucocutaneous blistering disorder epidermolysis bullosa acquisita ( EBA ), we found in this study a profound T‐ and B‐cell response along with an altered cytokine expression profile in draining lymph nodes of mice injected with the xenogeneic IgG. This was associated with the formation of circulating and skin‐bound mouse anti‐rabbit IgG in wild‐type but not CD 154‐deficient or B‐cell‐deficient JHT mice challenged with pathogenic rabbit IgG. Development of EBA skin lesions was attenuated in the two mouse strains lacking a B‐cell response at later observation time points, but was not affected in mice treated with the T‐cell trafficking blocker FTY 720. Collectively, our results implicate a host's xenoreactive immune response to rabbit anti‐mouse COL 7 IgG, a confounding effect that may contribute to immune complex‐driven inflammation and tissue damage in this antibody transfer‐induced EBA mouse model, especially at later time points. In this regard, it may be recommended to finish the evaluation of results obtained by experiments employing antibody‐transferred mouse models within the first 2 weeks after the pathogenic antibody injection.