| First Author | Osman GE | Year | 1998 |
| Journal | Int Immunol | Volume | 10 |
| Issue | 11 | Pages | 1613-22 |
| PubMed ID | 9846690 | Mgi Jnum | J:118789 |
| Mgi Id | MGI:3700403 | Doi | 10.1093/intimm/10.11.1613 |
| Citation | Osman GE, et al. (1998) Expression of a type II collagen-specific TCR transgene accelerates the onset of arthritis in mice. Int Immunol 10(11):1613-22 |
| abstractText | Animal models of autoimmune diseases have been instrumental in advancing our understanding of autoimmunity in humans. Collagen-induced arthritis in mice is an autoimmune disease model of rheumatoid arthritis, which is MHC class II restricted and CD4 T cell dependent. To better understand the fundamental role of T cells in arthritis, we have generated a transgenic mouse carrying the rearranged Valpha11.1 and Vbeta8.2 TCR chain genes isolated from a type II collagen (CII)-specific T cell hybridoma. Cell surface analysis indicated that Vbeta8.2 chain was expressed on the surface of nearly all peripheral T cells. Analysis of T cell subsets in transgenic mice revealed a profound skewing in peripheral T cells towards the CD4 population. Although peripheral T cells were not tolerant to CII and responded to CII stimulation in vitro, transgenic mice did not develop spontaneous arthritis. However, a rapid onset of arthritis with severe clinical signs was detected in transgenic mice after immunization with CII in complete Freund's adjuvant. Histological analysis of inflamed joints showed a great resemblance to arthritic joints in man. This unique transgenic mouse model provides valuable insights into the mechanism of arthritis and into potential specific immune interventions. |
