| First Author | Buxbaum J | Year | 2008 |
| Journal | J Autoimmun | Volume | 31 |
| Issue | 3 | Pages | 208-15 |
| PubMed ID | 18513923 | Mgi Jnum | J:314920 |
| Mgi Id | MGI:6828943 | Doi | 10.1016/j.jaut.2008.04.015 |
| Citation | Buxbaum J, et al. (2008) Hepatitis resulting from liver-specific expression and recognition of self-antigen. J Autoimmun 31(3):208-15 |
| abstractText | Liver-specific immune reactivity in response to aberrant expression of antigen on the surface of hepatocytes is thought to be a major factor in development of autoimmune hepatitis (AIH). Persistent inflammation develops when these antigens are not eliminated and/or responses are not appropriately regulated. We have developed transgenic mice (OVA-HEP), which express chicken ovalbumin on the surface of hepatocytes. These mice are tolerant to ovalbumin, develop normally and have shown no evidence of liver or other disease up to 2 years of age. Adoptive transfer of naive ovalbumin-specific T cells into OVA-HEP transgenic mice led to liver-specific inflammation in a dose dependent manner. This hepatic necroinflammation was dependent upon CD8(+) Valpha2 OVA-specific T cells, was limited to the liver, and was augmented by OVA-specific CD4(+) T cell help; but did not result from adoptive transfer of ovalbumin-specific CD4 T cells alone. The response was self-limited but persistent inflammation developed after repeated transfer of antigen-specific T cells. This model of T cell recognition of antigen on hepatocytes may be used to understand many liver-specific aspects of the immune response in autoimmune hepatitis. |
