Archives of Dermatological Research

, Volume 310, Issue 6, pp 533–533 | Cite as

Can such an animal model truly represent Henoch–Schönlein purpura?

  • Fengying Wang
  • Ruyue Chen
  • Xiaozhong LiEmail author
  • Yunyan Shen
Letter to the Editor

Dear Editor,

We read the article entitled “Histopathological and immunological changes during the acute and recovery phase in Henoch–Schönlein purpura rabbit model” published in Arch Dermatol Res with great interest [3]. Animal models are of great value in studying the pathogenesis of diseases. Literature on Henoch–Schönlein purpura (HSP) animal models is scarce; therefore, we consider that researches on exploring Henoch–Schönlein purpura animal model are very valuable.

Although the work they did makes a great contribution to the research on HSP models, the model needs to be further improved to truly represent Henoch–Schönlein purpura.

There are some key issues that need to be explored in the paper, which is critical to the success of the model. It has become the consensus that Henoch–Schönlein purpura, now called IgA vasculitis, is a kind of leukocyte rupture vasculitis mediated by immunoglobulin A-dominant immune complex affecting small vessels, and often involves skin, gastrointestinal tract, joints, and kidney [2].

Firstly, whether there was IgG and IgM deposition in skin and kidney tissue had not been explored. They only detected the deposition of IgA and C3, which was seen in the method section in the article “…and immunofluorescence staining was used for the detection of IgA, and C3 in the skin and kidney with specific antibodies (anti rabbit IgA-FITC, anti rabbit C3-FITC, MP-cappel).” Therefore, the study was not able to determine whether IgA deposition was predominated among three immunoglobulin (IgG, IgA, IgM), then nor was it possible to determine whether the model was an HSP model.

In the second place, the skin lesion of the model animal was caused by local irritation of the skin, rather than spontaneous purpura-like skin lesions as HSP patients, so it was not able to simulate the spontaneous clinical manifestations of HSP.

In addition, the majority of experimental animal species do not express IgA receptor FcαRI, which omits the effects of neutrophil activation via FcαRI [1]. So, it is not clear whether these models are representatives to study the pathomechanisms of HSP.


  1. 1.
    Heineke MH, Ballering AV, Jamin A, Ben MS, Monteiro RC, Van Egmond M (2017) New insights in the pathogenesis of immunoglobulin a vasculitis (Henoch–Schonlein purpura). Autoimmun Rev 16:1246–1253CrossRefPubMedGoogle Scholar
  2. 2.
    Jennette JC, Falk RJ, Bacon PA, Basu N, Cid MC, Ferrario F, Flores-Suarez LF, Gross WL, Guillevin L, Hagen EC, Hoffman GS, Jayne DR, Kallenberg CG, Lamprecht P, Langford CA, Luqmani RA, Mahr AD, Matteson EL, Merkel PA, Ozen S, Pusey CD, Rasmussen N, Rees AJ, Scott DG, Specks U, Stone JH, Takahashi K, Watts RA (2013) 2012 revised international chapel hill consensus conference nomenclature of vasculitides. Arthritis Rheum 65:1–11CrossRefPubMedGoogle Scholar
  3. 3.
    Li Y, Sui X, Zhu H, Xu Y, Huang L, Xu Y, Han Y, Feng X, Qin C (2017) Histopathological and immunological changes during the acute and recovery phase in Henoch–Schonlein purpura rabbit model. Arch Dermatol Res 309:21–30CrossRefPubMedGoogle Scholar

Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  • Fengying Wang
    • 1
    • 2
  • Ruyue Chen
    • 1
  • Xiaozhong Li
    • 1
    Email author
  • Yunyan Shen
    • 1
  1. 1.Department of Nephrology and RheumatologyChildren’s Hospital of Soochow UniversitySuzhouChina
  2. 2.Department of PediatricsAffiliated Taixing Hospital of Yangzhou UniversityTaixingChina

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