Animal models of behçet syndrome

Idan Goldberg, Ehud Baharav, Abraham Weinberger, Ilan Krause*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Animal models for Behçet syndrome (BS) can be divided according to the proposed etiological paradigms. These include environmental pollution and infectious (bacterial and viral) models, as well as various autoimmune and transgenic animal models. The environmental pollution model, though resembles the multisystem symptoms of BS, has limitations to become utilized as a model for the disease since it is difficult to produce, and the onset of symptoms appears erratically in a wide time range. The Streptococcal models have similarity only to the eye involvement in BS. This model is simple to induce with high rate of homogeneity. The HSV model has multisystem manifestations resembling BS; it has a moderate reproducibility. The autoimmune models utilizing S-Ag and IRBP are monosymptomatic models of BS-like uveitis. Those models are easy to induce, and extensive studies elucidated some of the immunological characteristics of BS including the paradigm of anti-HLA autoimmunity. The α-tropomyosin model shares some clinical features of BS. This model has a potential to become a useful autoimmune model for BS. The only published trial to establish a transgenic model for BS did not show any significant similarity to the human disease except a hyper-responsiveness of neutrophils.

Original languageEnglish
Title of host publicationBehçet Syndrome
PublisherSpringer International Publishing
Number of pages8
ISBN (Electronic)9783030241315
ISBN (Print)9783030241308
StatePublished - 1 Jan 2019


  • Air pollution
  • Animal model
  • Autoimmunity
  • Behçet syndrome
  • Heat shock proteins
  • Herpes simplex
  • Infectious
  • Uveitis


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