ABSTRACT
Minor histocompatibility (H ) antigens were first defined at the cellular level approximately 50 years ago.1,2 Since then, over 50 distinct H loci have been identified based upon their inheritance and segregation patterns in recombinant and congenic mouse strains. Polymorphisms in the H antigens account for the immunological responses that lead to graft rejection and graft versus host disease (GVHD) when tissue is transplanted between M HC identical individuals.3 The gene products of H loci serve as precursors of processed peptides which are presented by M HC molecules to T cells.4 The graft rejection phenotype resulting from differences between H loci, therefore, is the result o f T-cell responses elicited by either qualitative or quantitative differences in the antigenic peptides displayed by the M H C molecules on the donor versus the host cell surface. Identification of H antigens at the molecular level is thus critical for defining the basis of these genetic polym orphism s and is im portant for understanding the mechanisms by which graft rejection occurs.
