Tropomyosin-induced arthritis in rats

Ehud Baharav, Felix Mor, Marisa Halpern, Francisco Quintana, Abraham Weinberger*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Objective. Immunization of rats with ct-tropomyosin (TPM) led to arthritis, uveitis and dermatitis, typical features of Behçet's disease (BD). The present study characterizes the arthritic features of this animal model, not previously described. Methods. Lewis rats were immunized with bovine α-TPM and another group of rats was treated with neutralizing anti- tumor necrosis factor-α (TNF-α) antibodies. Results. Clinically more than 90% of the immunized rats developed severe acute arthritis 12 days after vaccination. Rats that were followed-up for 6 months had persistent inflammation of the leg joints. Histologic studies demonstrated predominant mononuclear infiltrations in the acute phase of arthritis; the chronic arthritic process resulted in cartilage and bone damage and abundant fibrosis which led to joint deformations. Male and female rats had a similar clinical course. Analysis of the splenocyte cytokine profile kinetics revealed a persistently high level of interferon-gamma (INF-γ) and an increase in TNF-α secretion during the acute phase. Increasing levels of interleukin (IL -10 heralded the decline in clinical arthritis. No IL-4 was detected. No arthritis was detected in the rats treated with anti-TNF-α antibodies. Conclusion. The data indicates that α-TPM serves as an autoantigen to induce acute and chronic destructive arthritis in rats. This model is a TNF-α dependent autoimmune disease, with a Th1 cytokine profile.

Original languageEnglish
Pages (from-to)S-86-S-92
JournalClinical and Experimental Rheumatology
Issue number4 SUPPL. 45
StatePublished - Jul 2007


  • Anti-tumor necrosis factor-α
  • Arthritis
  • Cytokines
  • Tropomyosin


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