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.
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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.)
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Chemical References |
- B7-1 Antigen
- B7-H1 Antigen
- Blood Proteins
- Cd274 protein, mouse
- Membrane Glycoproteins
- Peptides
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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
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