| anti-Müllerian hormone | |
| Hgncid: | 464 |
| Symbol: | AMH |
| Entrezgene: | 268 |
| Omim: | 600957 |
| Refseq: | NM_000479 |
| Uniprot: | P03971 |
| Chromosome: | 19 |
| Arm: | p |
| Band: | 13.3 |
| Lysine-Specific Demethylase 5D protein | |
| Hgncid: | 11115 |
| Symbol: | KDM5D |
| Altsymbols: | HYA, SMCY |
| Omim: | 426000 |
| Refseq: | NM_004653 |
| Uniprot: | Q9BY66 |
| Chromosome: | Y |
| Arm: | q |
| Band: | 11.223 |
| Male Enhanced Antigen 1 | |
| Hgncid: | 6986 |
| Symbol: | MEA1 |
| Altsymbols: | HYS |
| Omim: | 143170 |
| Refseq: | NM_001318942 |
| Uniprot: | Q16626 |
| Chromosome: | 6 |
| Arm: | p |
| Band: | 21.1 |
H-Y antigen is a male tissue specific antigen. Originally thought to trigger the formation of testes (via loci, an autosomal gene that generates the antigen and one that generates the receptor)[1] it is now known that it does not trigger the formation of testes but may be activated by the formation of testes.
There are several antigens which qualify as H-Y as defined by rejection of male skin grafts in female hosts or detected by cytotoxic T cells or antibodies. One H-Y, secreted by the testis, defined by antibodies, is identical to Müllerian-inhibiting substance (AMH gene). Another H-Y, minor histocompatibility antigen, seemed to be encoded in the SMCY gene (acronym for 'selected mouse cDNA on Y'), later identified as an 11-residue peptide from the Lysine-Specific Demethylase 5D protein (KDM5D gene) presented by HLA-B7. A third example is MEA1.
It has been shown that male mice lacking in the H-Y antigen, hence lacking in the gene producing it, have also lost genetic information responsible for spermatogenesis. This result also identified a gene on the mouse Y chromosome, distinct from the testis-determining gene, that was essential for spermatogenesis, thus raising the possibility that the very product of this "spermatogenesis gene" is the H-Y antigen.
Among humans, it has been observed that men with more older brothers tend to have a higher chance of being homosexual (see Fraternal birth order and male sexual orientation). For every additional older brother, a man's chance of being homosexual can rise by up to 33%.[2] One theory to explain this involves H-Y antigens, which suggests that a maternal immune reaction to these antigens has, to an extent, an inhibitory effect on the masculinization of the brain, and therefore, the more male foetuses that the mother of a man has had, the greater the maternal immune response towards him[3] and thus the greater the inhibitory effect on brain masculinization, which is believed to be a factor in sexual orientation.[2]
This hypothesis is supported by evidence that older sisters have no discernible influence on the sexual orientation of later-born males, which would be expected since H-Y antigen is male tissue specific, the 'probable involvement of H-Y antigen in the development of sex-typical traits, and the detrimental effects of immunization of female mice to H-Y antigen on the reproductive performance of subsequent male offspring'. More specifically, recent research (Jan 2018) has found maternal antibodies to the neuroligin NLGN4Y protein, a Y-chromosome protein important in male fetal brain development, to be involved in the fraternal birth order effect.[4]