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EMBRYONIC STEM CELLS: CHARACTERIZATION SERIES

Immunogenicity and Engraftment of Mouse Embryonic Stem Cells in Allogeneic Recipients

^aRoy J. and Lucille A. Carver College of Medicine, University of Iowa and Department of Veterans Affairs Medical Center;
^bImmunology Graduate Program, Iowa City, Iowa, USA

Key Words. Embryonic stem cells • Engraftment • Apoptosis • Mixed chimerism • Retinoic acid early inducible-1

Correspondence: Nicholas Zavazava, M.D., Ph.D., University of Iowa Hospitals and Clinics, Department of Internal Medicine, 200 Hawkins Drive, C51-F, Iowa City, Iowa 52242, USA. Telephone: 319-384-6577; Fax: 319-356-8280; e-mail: Nicholas-zavazava{at}uiowa.edu

Received January 11, 2006; accepted for publication June 16, 2006.
First published online in STEM CELLS EXPRESS   June 22, 2006.



Embryonic stem cells (ESCs) are pluripotent and therefore able to differentiate both in vitro and in vivo into specialized tissues under appropriate conditions, a property that could be exploited for cellular therapies. However, the immunological nature of these cells in vivo has not been well understood. In vitro, mouse-derived ESCs fail to stimulate T cells, but they abrogate ongoing alloresponses by a process that requires cell-cell contact. We further show that despite a high expression of the NKG2D ligand retinoic acid early inducible-1 by mouse ESCs, they remain resistant to natural killer cell lysis. In vivo, allogeneic mouse ESCs populate the thymus, spleen, and liver of sublethally irradiated allogeneic host mice, inducing apoptosis to T cells and establishing multilineage mixed chimerism that significantly inhibits alloresponses to donor major histocompatibility complex antigens. Immunohistochemical imaging revealed a significant percentage of ESC-derived cells in the splenic marginal zones, but not in the follicles. Taken together, the data presented here reveal that nondifferentiated mouse embryonic stem cells are non-immunogenic and appear to populate lymphoid tissues in vivo, leading to T-cell deletion by apoptosis.

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