Disease relevance of JARID1D

• The presence of H-Y antibodies correlated with chronic graft-versus-host disease (GVHD) by univariate (odds ratio [OR] = 15.5; P < .0001) and multivariable logistic regression analysis (OR = 56.5; P < .0001) [1].
• The clinical significance of H-Y antibodies was characterized in 75 male patients with hematologic malignancies who received stem cells from female donors (F --> M HSCT) [1].
• Use of HLA-DQ5-expressing female Epstein-Barr virus transformed B lymphoblastoid cell lines transfected with various H-Y genes and loaded with overlapping peptides demonstrated that both T cell clones are specific for a peptide encoded by DDX3Y [2].
• Sensitisation to antigens expressed by bile-duct epithelium as in primary biliary cirrhosis or exposure to donor bile-duct minor histocompatibility antigens, such as the male sex related H-Y antigen, may provide an explanation [3].
• In haplotype analysis, the HYD haplotype was associated with increased risk of stomach cancer when compared with HYA, the most common haplotype (OR = 1.9, 95% CI 1.1-3.2; p = 0.021) [4].

Psychiatry related information on JARID1D

• The relevance of H-Y antigen for the aetiology of transsexualism is discussed [5].

High impact information on JARID1D

• In vitro T cell responses to H-Y are controlled by MHC class I and II Ir genes, which-respectively, restrict CD8 and CD4 T cells: These can be isolated as T cell clones in vitro [6].
• In vivo primary skin graft responses to H-Y are controlled by immune response (Ir) genes mapping to the MHC [6].
• T cell receptor (TCR) transgenic mice have been made from the rearranged TCR genes of several of these, of which that specific for H-Y/Db is the best studied [6].
• In mice transfection of cosmids and cDNAs mapping to the Sxrb deletion has identified two genes encoding H-Y peptide epitopes [6].
• The current serological study revealed the presence in XO males and the absence from XO females of H-Y (histocompatibility Y) antigen [7].

Chemical compound and disease context of JARID1D

• To compare six assays of hyaluronan (hyaluronic acid; HYA) in serum, developed in different laboratories, we analyzed 10 samples from each of three groups: healthy persons, patients with primary biliary cirrhosis, and patients with rheumatoid arthritis [8].

Biological context of JARID1D

• Primary genomic sequencing determined gene SMCY to be composed of 27 exons that comprise 4,620 bp of coding sequence [9].
• Previously, 2 human H-Y epitopes derived from the same SMCY gene have been identified that were involved in bone marrow graft rejection [10].
• The H-Y phenotype is normally associated with the male sex in mammals [11].
• Antibody responses to H-Y minor histocompatibility antigens correlate with chronic graft-versus-host disease and disease remission [1].
• Similarly, Y chromosome locus order was remarkably conserved between cat and human Y chromosomes, with only one marker (SMCY) position rearranged between the species [12].

Anatomical context of JARID1D

• Moreover, all cytotoxic T lymphocytes tested (n=6) were specific for the SMCY-derived peptide FIDSYICQV, originally described as being the H-Y epitope recognized in the context of HLA-A*0201 [13].
• H-Y antigen has been defined by various immunological methods including graft rejection, T-cell mediated cytolysis, and antiserum cytotoxicity [11].
• Anti-H-Y antisera detect a membrane bound antigen associated with beta2-microglobulin, and a soluble protein secreted by testicular Sertoli cells [11].
• H-Y is a transplantation antigen that can lead to rejection of male organ and bone marrow grafts by female recipients, even if the donor and recipient match at the major histocompatibility locus of humans, the HLA (human leukocyte antigen) locus [14].
• In contrast to the SMCY-encoded H-Y epitopes, the B8/H-Y Ag was not presented by fibroblasts from male donors, suggesting that it was encoded by a novel gene [15].

Associations of JARID1D with chemical compounds

• Cutting edge: the HLA-A*0101-restricted HY minor histocompatibility antigen originates from DFFRY and contains a cysteinylated cysteine residue as identified by a novel mass spectrometric technique [16].
• Although arginine at position 2 is a dominant anchor residue for peptides bound to B27, neither B27-presented HY sequence contains this residue [17].
• In non-mammalian vertebrates, H-Y antigen is controlled by other factors, e.g. steroid hormones [18].
• The increase in the thickness of the epidermal HYA meshwork after 6 months and the blister fluid HYA after 2 weeks may indicate that HYA is involved in the epidermal change induced by topical retinoic acid therapy.(ABSTRACT TRUNCATED AT 250 WORDS)[19]
• This study was undertaken with the aim of localizing hyaluronan (hyaluronic acid, HYA) in tissue sections of the human endolymphatic sac by use of a hyaluronan-binding affinity protein and the avidin-biotin/peroxidase staining procedure [20].

Regulatory relationships of JARID1D

• The human homologues SMCY and UTY likewise express HY antigens and these are targets of damaging graft-versus-host (GVH) responses and potentially therapeutic graft-versus-leukaemia (GVL) responses following bone marrow transplantation (BMT) [21].

Other interactions of JARID1D

• Analysis of mutation rates in the SMCY/SMCX genes shows that mammalian evolution is male driven [22].
• The UTY-derived H-Y antigen was characterized as a 10-amino acid residue peptide, RESEEESVSL [23].
• All previously identified H-Y Ags are encoded by conventional open reading frames, but we report in this study the identification of a novel H-Y Ag encoded in the 5'-untranslated region of the TMSB4Y gene [24].
• Although the epitope differed by 3 amino acids from its X-homologue, UTX, only 2 polymorphisms were essential for recognition by the CTL clone HLA-B60 HY [23].
• However, A1-HY-specific CTL recognize the DFFRY-derived peptide at a 1500-fold lower dose than the female homologue [16].

Analytical, diagnostic and therapeutic context of JARID1D

• H-Y antibodies develop 4 to 12 months after transplantation and persist for long periods [1].
• The identification of H-Y may aid in transplantation prognosis, prenatal diagnosis, and fertilization strategies [14].
• Acute antibody-mediated rejection (AAR) of mouse skin allografts was studied in nine donor-recipient combinations with increasing histoincompatibility ranging from an H-Y to a complete H-2 plus on-H-2 disparity [25].
• All the assays are based on the use of affinity proteins specific for HYA, prepared from cartilage or brain tissue, and are analogous to RIA or enzyme immunoassay techniques [8].
• Purified HLA-A2.1 molecules obtained by affinity chromatography of 6 x 10(10) Epstein Barr virus (EBV)-transformed B lymphocytes were used in an attempt to isolate the human HLA-A2.1-restricted minor histocompatibility (H) peptides H-Y and HA-2 [26].

References