Linkage of Mls genes to endogenous mammary tumour viruses of inbred mice.
T cells that recognize self antigen are clonally deleted in the thymus--a maturation process that occurs in the context of histocompatibility molecules and the T-cell receptor. The minor lymphocyte stimulation antigens (Mls) effect these deletions through interactions with the V beta portion of the T-cell receptor, thus mimicking bacterial 'superantigens'. Intrigued by the fact that each known Mls gene maps to the same chromosomal region as an endogenous mouse mammary tumour virus (Mtv), we reevaluated the linkage relationships between the two gene families. Here we report perfect concordance in inbred and recombinant inbred mice between the presence of four Mtv proviruses with the expression of Mls gene products. These data suggest a general model in which mammary tumour virus gene products themselves are the ligands that shape a considerable portion of the immunological repertoire of common laboratory mice.
Frankel
W N
WN
Department of Molecular Biology, Tufts University School of Medicine, Boston, Massachusetts 02111.
Rudy
C
C
Coffin
J M
JM
Huber
B T
BT
D000818:Animals; D000954:Antigens, Surface / Q000235:genetics*; D015139:Blotting, Southern; D002874:Chromosome Mapping; D008040:Genetic Linkage; D008324:Mammary Tumor Virus, Mouse / Q000235:genetics*; D051379:Mice; D008815:Mice, Inbred Strains; D016747:Minor Lymphocyte Stimulatory Antigens; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D016693:Receptors, Antigen, T-Cell, alpha-beta; D013601:T-Lymphocytes / Q000276:immunology*
D000954:Antigens, Surface; D016747:Minor Lymphocyte Stimulatory Antigens; D011948:Receptors, Antigen, T-Cell; D016693:Receptors, Antigen, T-Cell, alpha-beta