TY - JOUR
T1 - B7-H1 determines accumulation and deletion of intrahepatic CD8+ T lymphocytes
AU - Dong, Haidong
AU - Zhu, Gefeng
AU - Tamada, Koji
AU - Flies, Dallas B.
AU - Van Deursen, Jan M.A.
AU - Chen, Lieping
N1 - Funding Information:
We thank Andrew S. Flies and Julie S. Lau for their excellent technical assistance, Kathryn A. Jensen and Julie S. Lau for editing the manuscript, and other members of this laboratory for discussions. This work was supported by the Mayo Foundation and the National Institutes of Health grants CA98721, CA97085, and CA85721.
PY - 2004/3
Y1 - 2004/3
N2 - 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.
AB - 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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U2 - 10.1016/S1074-7613(04)00050-0
DO - 10.1016/S1074-7613(04)00050-0
M3 - Article
C2 - 15030776
AN - SCOPUS:1642306942
SN - 1074-7613
VL - 20
SP - 327
EP - 336
JO - Immunity
JF - Immunity
IS - 3
ER -