NDLI: Liver sinusoidal endothelial cells contribute to CD8 T cell tolerance toward circulating carcinoembryonic antigen in mice.

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Liver sinusoidal endothelial cells contribute to CD8 T cell tolerance toward circulating carcinoembryonic antigen in mice.

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Liver sinusoidal endothelial cells contribute to CD8 T cell tolerance toward circulating carcinoembryonic antigen in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Höchst, Bastian Schildberg, Frank A. Böttcher, Jan Metzger, Christina Huss, Sebastian Türler, Andreas Overhaus, Markus Knoblich, Andreas Schneider, Berthold Pantelis, Dimitrios Kurts, Christian Kalff, Jörg C. Knolle, Percy Diehl, Linda
Description	Country affiliation: Germany Author Affiliation: Höchst B ( Institutes of Molecular Medicine and Experimental Immunology, University of Bonn, Germany.)
Abstract	UNLABELLED: Immunity against cancer is impeded by local mechanisms promoting development of tumor-specific T cell tolerance, such as regulatory T cells, myeloid-derived suppressor cells, or immunosuppressive factors in the tumor microenvironment. The release of soluble antigens, such as carcinoembryonic antigen (CEA) from colorectal carcinoma (CRC) cells, has been investigated for diagnostic purposes, but not for its immunological consequences. Here, we address the question of whether soluble CEA influences tumor-specific immunity. Mice were injected with soluble CEA protein, and CEA-specific CD8 T cells were analyzed for their phenotype and functionality by means of restimulation ex vivo or antitumor efficacy in vivo. We furthermore characterized the CD8 T cell population in peripheral blood mononuclear cell (PBMCs) from healthy donors and colorectal carcinoma patients. In mice, circulating CEA was preferentially taken up in a mannose receptor-dependent manner and cross-presented by liver sinusoidal endothelial cells, but not dendritic cells, to CD8 T cells. Such systemically circulating CEA promoted tolerization of CEA-specific CD8 T cells in the endogenous T cell repertoire through the coinhibitory molecule B7H1. These CD8 T cells were not deleted but were rendered nonresponsive to antigen-specific stimulation and failed to control growth of CEA-expressing tumor cells. These nonresponsive CD8 T cells were phenotypically similar to central memory T cells being CD44(high) CD62L(high) CD25(neg) . We found T cells with a similar phenotype in PBMCs of healthy donors and at increased frequency also in patients with colorectal carcinoma. CONCLUSION: Our results provide evidence for the existence of an unrecognized tumor immune escape involving cross-presentation of systemically circulating tumor antigens that may influence immunotherapy of cancer.
File Format	HTM / HTML
ISSN	02709139
Issue Number	5
Volume Number	56
e-ISSN	15273350
Journal	Hepatology
Language	English
Publisher	Wiley
Publisher Date	2012-11-01
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Discipline Hepatology Cd8-positive T-lymphocytes Immunology Carcinoembryonic Antigen Carcinoma Colorectal Neoplasms Endothelial Cells Immune Tolerance Liver Animals Antigen-presenting Cells Antigens, Cd274 Metabolism Antigens, Cd44 Blood Humans Interleukin-2 Receptor Alpha Subunit L-selectin Leukocytes, Mononuclear Lymphocyte Count Mice Mice, Transgenic Phenotype Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Hepatology

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