| First Author | Bhan AK | Year | 2000 |
| Journal | Int Rev Immunol | Volume | 19 |
| Issue | 1 | Pages | 123-38 |
| PubMed ID | 10723681 | Mgi Jnum | J:61252 |
| Mgi Id | MGI:1354612 | Doi | 10.3109/08830180009048393 |
| Citation | Bhan AK, et al. (2000) Spontaneous chronic colitis in TCR alpha-mutant mice; an experimental model of human ulcerative colitis. Int Rev Immunol 19(1):123-38 |
| abstractText | Mice with targeted disruption of the T cell receptor alpha gene (TCR alpha-/-) spontaneously develop chronic colitis. Colonic inflammation begins at 6-8 weeks of age and chronic colitis is established in about 60% of mice by 16-20 weeks of age. The disease is also associated with autoantibodies (anti-tropomyosin antibodies, anti-neutrophil cytoplasmic antibodies) and an oligoclonal immune response to luminal bacterial antigens. Although T cells, but not B cells or autoantibodies, are essential for the development of colitis, B cells and/or autoantibodies may have a regulatory role in the pathogenesis of this colitis because the colitis is more severe in B cell deficient TCR alpha-/- mice. Cytokines, specifically IL-4 and IL-1, also play an important role in the development of colitis in TCR alpha-/- mice. Enteric bacteria located in the large intestine are an important factor in the pathogenesis of this colitis because germ-free TCR alpha-/- mice do not develop colitis and appendectomy at an early age delays the onset of this colitis. The colitis in TCR alpha-/- mice resembles human ulcerative colitis and provides a useful model to study the pathogenesis of human inflammatory bowel disease. |
