The Journal of Experimental Medicine
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Published online 12 May 2003 doi:10.1084/jem.20030044
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© Rockefeller University Press, 0022-1007/2003/5/1279 $5.00
The Journal of Experimental Medicine, Volume 197, Number 10, 1279-1289

A Human Minor Histocompatibility Antigen Resulting from Differential Expression due to a Gene Deletion

Makoto Murata1,2, Edus H. Warren1,2 and Stanley R. Riddell1,2

1 Program in Immunology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109
2 Division of Oncology, University of Washington, Seattle, WA 98104

Address correspondence to Dr. Stanley Riddell, D3-100, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA 98109. Phone: 206-667-5249; Fax: 206-667-7983; E-mail: sriddell{at}fhcrc.org

Minor histocompatibility antigens (minor H antigens) are targets of graft-versus-host disease and graft-versus-leukemia responses after allogeneic human leukocyte antigen identical hematopoietic stem cell transplantation. Only a few human minor H antigens have been molecularly characterized and in all cases, amino acid differences between homologous donor and recipient proteins due to nucleotide polymorphisms in the respective genes were responsible for immunogenicity. Here, we have used cDNA expression cloning to identify a novel human minor H antigen encoded by UGT2B17, an autosomal gene in the multigene UDP-glycosyltransferase 2 family that is selectively expressed in liver, intestine, and antigen-presenting cells. In contrast to previously defined human minor H antigens, UGT2B17 is immunogenic because of differential expression of the protein in donor and recipient cells as a consequence of a homozygous gene deletion in the donor. Deletion of individual members of large gene families is a common form of genetic variation in the population and our results provide the first evidence that differential protein expression as a consequence of gene deletion is a mechanism for generating minor H antigens in humans.

Key Words: hematopoietic stem cell transplantation • graft-versus-host disease • cytotoxic T lymphocyte • UDP glycosyltransferase 2B family • cDNA expression cloning


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