An H–YDb epitope is encoded by a novel mouse Y chromosome gene

Abstract

Rejection of male tissue grafts by genotypically identical female mice has been explained by the existence of a male-specific transplantation antigen, H-Y (ref. 1), but the molecular nature of H-Y antigen has remained obscure. Hya, the murine locus controlling H-Y expression, has been localized to delta Sxrb, a deletion interval of the short arm of the Y chromosome. In mice, H-Y antigen comprises at least four distinct epitopes, each recognized by a specific T lymphocyte clone. It has recently been shown that one of these epitopes, H-YKk, is a peptide encoded by the Y-linked Smcy gene, presented at the cell surface with the H-2Kk major histocompatibility complex (MHC) molecule. However, deletion mapping and the analysis of variable inactivation of H-Y epitopes has suggested that the Hya locus may be genetically complex. Here we describe a novel mouse Y chromosome gene which we call Uty (ubiquitously transcribed tetratricopeptide repeat gene on the Y chromosome). We identify the peptide WMHHNMDLI derived from the UTY protein as an H-Y epitope, H-YDb. Our data formally demonstrate that H-Y antigen is the product of more than one gene on the Y chromosome.

Bone marrow mesenchymal stem cells induce division arrest anergy of activated T cells

“…Stimulator cells were pulsed with 1000 ng/mL K k -restricted (TENSGKDI) HY peptide 20 (encoded by the Smcy gene) or with the D b -restricted Smcy (KCSRNRQYL), 23 the Uty (WMHHNMDLI) 24 encoded, and the A brestricted Dby encoded (NAGFNSNRANSSRSS) 25 HY peptides at 37°C for 2 hours. Unpulsed irradiated CBA or C57BL/6 female splenocytes were used as negative controls.…”

Anergic T Cells Inhibit the Antigen-Presenting Function of Dendritic Cells

“…CTL10 is an H-Y-specific, H2-D b -restricted CD8 ϩ T cell clone (16). All T cell clones were maintained in RPMI 1640 medium supplemented with 10% FCS (Globepharm, Esher, U.K.), 2 mM L-glutamine, 100 U/ml penicillin, 100 g/ml streptomycin, and 5 ϫ 10 Ϫ5 M 2-ME, in the presence of rhIL-2 (10 U/ml for CD4 ϩ and 20 U/ml for the CD8 ϩ cells) (Boehringer Mannheim, Mannheim, Germany).…”

The H4b Minor Histocompatibility Antigen Is Caused by a Combination of Genetically Determined and Posttranslational Modifications

“…5). The data thus far indicate that immune responses to minor H Ags could result from the recipient carrying a null allele (e.g., H60 and HY male Ag) (6,7) or differential or induced expression (e.g., H28) (8), differential processing (e.g., human minor H Ag HA8) (9), or amino acid sequence variation in the peptide epitope (e.g., H3 and H13) (10,11). Sequence variation is a consequence of evolving genomes.…”