1. ¹Section of Nephrology, Yale University School of Medicine, New Haven, Connecticut, USA
2. ²Department of Medicine and Center for Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, USA
3. ³Section of Medical Oncology, Yale University School of Medicine, New Haven, Connecticut, USA
4. ⁴Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
5. ⁵Department of Surgery, Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
6. ⁶Department of Immunology, Thomas E. Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
7. ⁷Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut, USA
8. ⁸Department of Dermatology, Yale University School of Medicine, New Haven, Connecticut, USA

Correspondence: Dr Daniel H. Kaplan, Department of Dermatology, Center for Immunology, University of Minnesota, 6-118 NHH, 312 Church St SE, Minneapolis, Minnesota 55455, USA. E-mail: dankaplan@umn.edu

⁹These authors contributed equally to this work

Received 16 March 2007; Accepted 28 January 2008; Published online 13 March 2008.

Abstract

The mechanism of skin allograft rejection has been thought to require presentation of graft antigen by resident epidermal Langerhans cells (LCs). We have previously engineered mice that have a selective and constitutive absence of epidermal LCs. By using donor skin from these LC-deficient mice, we show that LCs are not required for rejection of major (FVB B6) or minor (H-Y, male female on B6 background) antigen-mismatched skin grafts. On the FVB background, where H-Y mismatched grafts are normally maintained indefinitely, grafts lacking LCs are efficiently rejected. Thus, LCs in the donor graft are required for long-term skin engraftment, which supports a regulatory role for LCs in skin graft acceptance.

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