title: The H-mshi antigen is conserved among standard BALB/cBy, C57BL/6J, and wild-derived CAST/Ei and SPRET/Ei inbred strains of mice.
abstract: The recessive male sterility and histoincompatibility mutation (mshi) arose spontaneously in the standard inbred mouse strain BALB/cBy. In addition to generating sterility in homozygous males, mshi controls the loss of a minor histocompatibility antigen designated H-mshi. To determine whether the H-mshi antigen normally expressed by the BALB/cBy strain (H-mshi(c)) is the same as or different from the antigen (H-mshi(x)) expressed by the standard inbred C57BL/6J strain or the wild-derived CAST/Ei and SPRET/Ei strains, animals heterozygous for the mutant antigen-loss allele (H-mshi-) and H-mshi(x) were grafted with tail skin from BALB/cBy mice. The long-term retention of grafts by these hosts indicates that the H-mshi antigen encoded by the BALB/cBy, C57BL/6J, CAST/Ei, and SPRET/Ei strains is histogenically identical. Conservation of this minor histocompatibility antigen among these evolutionarily diverse strains suggests that H-mshi encodes a functionally important cellular product(s).
authors.affiliation: Department of Biological Sciences, Central Connecticut State University, 1615 Stanley Street, New Britain, CT 06050, USA.
authors.forename: A L
authors.initials: AL
authors.lastname: Hildebrandt
authors.forename: A M
authors.initials: AM
authors.lastname: Cantwell
authors.forename: M C
authors.initials: MC
authors.lastname: Rule
authors.forename: T R
authors.initials: TR
authors.lastname: King
mesh_terms: D000818:Animals; D000835:Animals, Wild; D005260:Female; D006084:Graft Rejection; D016130:Immunophenotyping; D007248:Infertility, Male / Q000235:genetics* / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D015778:Minor Histocompatibility Antigens / Q000235:genetics*; D016038:Skin Transplantation / Q000276:immunology
chemical_list: D015778:Minor Histocompatibility Antigens