ABSTRACT
Histoincompatibility was first detected in mice at the beginning of the 20th century. The great majority of the loci responsible for this complex genetic trait are located on the autosomal chromosomes. The ability to customize the mouse genome by the production of congenic stocks of mice that isolate individual histocompatibility (H ) loci has enormously simplified the analysis of the trait of histoincompatibility. Recent advances in molecular genetics are making it possible to define the minor H genes captured in congenic strains. Given the genetic and biological similarity of mice and humans, the molecular character ization of mouse H loci increases the value of the mouse model in developing approaches to improve the success of tissue transplantation between humans.
