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

Immunity. 2004 Mar;20(3):327-36. doi: 10.1016/s1074-7613(04)00050-0.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

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


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