| First Author | Dong H | Year | 2004 |
| Journal | Immunity | Volume | 20 |
| Issue | 3 | Pages | 327-36 |
| PubMed ID | 15030776 | Mgi Jnum | J:89781 |
| Mgi Id | MGI:3041391 | Doi | 10.1016/s1074-7613(04)00050-0 |
| Citation | Dong H, et al. (2004) B7-H1 determines accumulation and deletion of intrahepatic CD8(+) T lymphocytes. Immunity 20(3):327-36 |
| abstractText | Upon systemic activation by antigens, CD8(+), but not CD4(+), T cells selectively accumulate and undergo apoptosis in the liver, a mechanism associated with the induction of hepatic tolerance and chronic infection. The molecular basis for CD8(+) T cell preference in this process is unknown. We prepared B7-H1-deficient mice by gene targeting and found spontaneous accumulation of CD8(+) T cells in the liver while CD4(+) T cell levels remained normal. Moreover, antigen-driven CD8(+) T cells proliferated normally while apoptotic levels during the contraction phase was selectively impaired in the liver, leading to accelerated hepatocyte damage in experimental autoimmune hepatitis. Therefore, B7-H1 is a key protein selectively regulating the accumulation and deletion of intrahepatic CD8(+) T cells and may also contribute to inflammation, autoimmune diseases, and tolerance in the liver. |
