Abstract
The presence of recipient disparity for a minor histocompatibility antigen termed HA-1 is associated with an increased risk of grades II-IV GVHD after marrow transplantation from an HLA-identical sibling. These data offer an opportunity to test the validity of theoretical models suggesting that the minor antigens capable of eliciting GVHD in any given individual are encoded by approximately seven genetic loci. Published data and theoretical models agree that there is little benefit to be gained by typing and matching at a single locus. The models predict, however, that substantial benefit would be possible if multiple loci could be typed. The success of matching would be enhanced by the availability of assays that would allow typing for at least four of the loci encoding antigens that could cause GVHD in any given individual.

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