B7-H1 determines accumulation and deletion of intrahepatic CD8(+) T lymphocytes.

Abstract

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.

• Authors: Haidong Dong, Gefeng Zhu, Koji Tamada, Dallas B Flies, Jan M A van Deursen, Lieping Chen
• Journal: Immunity (Immunity) Vol. 20 Issue 3 Pg. 327-36 (Mar 2004) ISSN: 1074-7613 [Print] United States
• PMID: 15030776 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• B7-1 Antigen
• B7-H1 Antigen
• Blood Proteins
• Cd274 protein, mouse
• Membrane Glycoproteins
• Peptides

Topics

• Animals
• Apoptosis
• Autoimmune Diseases (immunology, pathology)
• B7-1 Antigen (genetics, physiology)
• B7-H1 Antigen
• Blood Proteins
• CD8-Positive T-Lymphocytes (immunology, pathology)
• Cell Movement
• Hepatitis, Animal (immunology, pathology)
• Kinetics
• Liver (cytology, immunology, pathology)
• Lymphocyte Activation
• Membrane Glycoproteins
• Mice
• Mice, Knockout
• Peptides