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  Skin microbiota-associated inflammation precedes autoantibody induced tissue damage in experimental epidermolysis bullosa acquisita

Ellebrecht, C. T., Srinivas, G., Bieber, K., Banczyk, D., Kalies, K., Künzel, S., et al. (2015). Skin microbiota-associated inflammation precedes autoantibody induced tissue damage in experimental epidermolysis bullosa acquisita. Journal of Autoimmunity, in press. doi:10.1016/j.jaut.2015.08.007.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-5B5E-3 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-5B5F-1
Genre: Journal Article

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 Creators:
Ellebrecht, Christoph T., Author
Srinivas, Girish1, Author              
Bieber, Katja, Author
Banczyk, David, Author
Kalies, Kathrin, Author
Künzel, Sven2, Author              
Hammers, Christoph M., Author
Baines, John F.1, Author              
Zillikens, Detlef, Author
Ludwig, Ralf J., Author
Westermann, Jürgen, Author
Affiliations:
1Guest Group Evolutionary Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445638              
2Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445635              

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Free keywords: autoimmune bullous disease; host-microbiome interaction; autoantibodies
 Abstract: Epidermolysis bullosa acquisita (EBA) is a chronic autoimmune blistering skin disease characterized by autoantibodies against type VII collagen (COL7). Immunization of SJL/J mice with recombinant murine COL7 results in break of tolerance and skin blisters. Strikingly, despite circulating autoantibodies, the same genetic background and identical environmental conditions, 20% of mice remain healthy. To elucidate the regulation of the transition from the presence of autoantibodies to overt autoimmune disease, we characterized the innate and adaptive immune response of mice that remain healthy after immunization and compared it to mice that developed skin disease. Both clinically healthy and diseased SJL/J mice showed circulating autoantibodies and deposition of complement-fixing IgG2c autoantibodies and C3 at the dermaleepidermal junction. However, only in diseased animals significant neutrophil infiltration and increase in FcgRIV expression were observed in the skin. In contrast, the expression of T cell signature cytokines in the T cell zone of the draining lymph node was comparable between clinically healthy and diseased animals after immunization. Surprisingly, health was associated with a decreased expression of CD11c, TNFA and KC (CXCL1) in the skin prior to immunization and could be predicted with a negative predictive value of >80%. Furthermore, mice that did not develop clinical disease showed a significantly higher richness and distinctly clustered diversity of their skin microbiota before immunization. Our data indicate that the decision whether blisters develop in the presence of autoantibodies is governed in the skin rather than in the lymph node, and that a greater richness of cutaneous bacterial species appears to be protective.

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Language(s): eng - English
 Dates: 2015-08-092014-08-242015-08-142015
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: -
 Identifiers: DOI: 10.1016/j.jaut.2015.08.007
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Title: Journal of Autoimmunity
  Other : J. Autoimmun.
Source Genre: Journal
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Publ. Info: London : Academic Press
Pages: 9 S. Volume / Issue: in press Sequence Number: - Start / End Page: - Identifier: ISSN: 0896-8411 (print)
ISSN: 0896-8411 (online)
ISSN: 1095-9157 (online)
CoNE: /journals/resource/954922649139