J Yeungnam Med Sci.  2023 Jan;40(1):23-29. 10.12701/jyms.2022.00773.

The use of animal models in rheumatoid arthritis research

Affiliations
  • 1Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul, Korea
  • 2Center for Integrative Rheumatoid Transcriptomics and Dynamics, College of Medicine, The Catholic University of Korea\, Seoul, Korea

Abstract

The pathological hallmark of rheumatoid arthritis (RA) is a synovial pannus that comprises proliferating and invasive fibroblast-like synoviocytes, infiltrating inflammatory cells, and an associated neoangiogenic response. Animal models have been established to study these pathological features of human RA. Spontaneous and induced animal models of RA primarily reflect inflammatory aspects of the disease. Among various induced animal models, collagen-induced arthritis (CIA) and collagen antibody-induced arthritis (CAIA) models are widely used to study the pathogenesis of RA. Improved transplantation techniques for severe combined immunodeficiency (SCID) mouse models of RA can be used to evaluate the effectiveness of potential therapeutics in human tissues and cells. This review provides basic information on various animal models of RA, including CIA and CAIA. In addition, we describe a SCID mouse coimplantation model that can measure the long-distance migration of human RA synoviocytes and cartilage destruction induced by these cells.

Keyword

Animal models; Invasion; Migration; Rheumatoid arthritis; Synoviocytes

Figure

  • Fig. 1. Schematic of model using synoviocyte migration in severe combined immunodeficiency mice. Skin inflammation was induced by subcutaneously injecting CFA (120 µg) into site a. One day after the CFA injection, rheumatoid arthritis-FLSs were implanted intradermally in site c. Five days after human FLSs implantation, skin samples were obtained from site b. CFA, complete Freund’s adjuvant; FLS, fibroblast-like synoviocyte.

  • Fig. 2. Schematic of model using synoviocyte migration and invasion SCID. Cartilage and rheumatoid arthritis-FLSs were coimplanted into SCID mice at the primary site and cartilage without cells was implanted at the contralateral site. After 60 days, the implants were removed, embedded in paraffin, and stained with hematoxylin and eosin (H&E). Implant evaluation was performed using H&E-stained sections to determine invasion and perichondrocytic cartilage degradation. SCID, severe combined immunodeficiency; FLS, fibroblast-like synoviocyte.


Reference

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