Disease relevance of H2-D1

• We have studied two murine embryonal carcinoma tumors, 402AX and PCC4, that are rejected in vivo immunologically, although they do not express H-2K or H-2D antigens [1].
• Expression of H-2K and H-2D genes by PYS-2 teratocarcinoma cells [2].
• In a series of newly isolated AKR leukemias, some tumors expressed large amounts of both H-2K and H-2D molecules, while others had reduced levels of both antigens [3].
• Experimental allergic orchitis in mice. VI. Recombinations within the H-2S/H-2D interval define the map position of the H-2-associated locus controlling disease susceptibility [4].
• It was found that only strains with b alleles between H-2S and H-2D had significantly higher frequencies of isolated cleft palate among their progeny when fed the supplemental vitamin A. The locus appears to be on the centromeric side of a dexamethasone-induced cleft palate gene which has been mapped to the same general area [5].

Psychiatry related information on H2-D1

• We show that in primary spontaneous AKR leukemias, in spite of large individual differences, the expression of high amounts of MuLV gp70 is not random, but is associated with high expression of H-2K and H-2D antigens [6].
• A unique immune response control locus mapping with the H-2D class I region [7].

High impact information on H2-D1

• At the centromeric end the t12 lethal maps between TL and H-2D in the Qa region, and distally the tw5 lethal is inseparable from H-2K [8].
• Examination of two other glycoproteins (the major histocompatibility complex antigens) in these cell lines showed that in M3.11, the H-2D but not the H-2K product was abnormally glycosylated and contained a smaller glycopeptide [9].
• However, in a subclone of M3.11 that had lost the ability to produce immunoglobulin heavy chains, the H-2D glycopeptide had returned to wild-type size [9].
• We concluded from these studies that the defective M3.11 immunoglobulin heavy chain interfered both with its own glycosylation and the glycosylation of another protein, H-2D [9].
• In previous experiments we have introduced the T-cell receptor alpha- and beta-chain genes from a CD8-positive cytolytic T cell specific for the antigen fluorescein (FL) and the H-2D molecule of the major histocompatibility complex (MHC) into a CD8-negative recipient cell [10].

Chemical compound and disease context of H2-D1

• Genetic restrictions for the induction of suppressor T cells by hapten-modified lymphoid cells in tolerance to 1-fluoro-2,4-dinitrobenzene contact sensitivity. Role of the H-2D region of the major histocompatibility complex [11].
• A gene that affects susceptibility to cortisone-induced cleft palate maps between H-2S and H-2D on mouse chromosome 17 [12].

Biological context of H2-D1

• Tumour necrosis factor and lymphotoxin genes map close to H-2D in the mouse major histocompatibility complex [13].
• Genetic mapping studies show that this cloned t-DNA is homologous to the H-2 D region of wild-type chromosomes, and that the E alpha Ia gene maps telomeric to this DNA fragment in t-haplotypes, in contrast to its orientation in wild-type chromosomes [14].
• The transplantation antigens H-2K, H-2D and H-2L are developmentally regulated, highly polymorphic cell surface proteins encoded by the major histocompatibility gene complex (MHC) [15].
• Molecular evidence that the H-2D and H-2L genes arose by duplication. Differences between the evolution of the class I genes in mice and humans [16].
• A complete DNA sequence of the H2-Dd gene shows that a variety of alternative splice sites exist throughout the gene, which may lead to additional gene products and may explain the multiplicity of H-2D-encoded polypeptides [17].

Anatomical context of H2-D1

• These findings illustrate the complexity of the chromosome segment between the H-2D and Tla loci and they emphasize the role of major histocompatibility complex-associated genes for the differentiation of T cells into different subpopulations with possibly distinct immunologic functions [18].
• Dendritic cell maturation overrules H-2D-mediated natural killer T (NKT) cell inhibition: critical role for B7 in CD1d-dependent NKT cell interferon gamma production [19].
• Cytotoxic anti-H-2D antibodies and complement were used to isolate 161 independent target antigen-negative clones from H-2d/H-2b heterozygous cell lines; of these, 131 (84.5%) lost the allele encoding the target antigen [20].
• Induction of the H-2 D antigen during B cell activation [21].
• Resistance maps to the H-2D gene and not to the H-2K gene and is associated with a potent antiviral cytotoxic T-lymphocyte (CTL) response [22].

Associations of H2-D1 with chemical compounds

• The progeny were assayed for H-2D markers, Pgk-2 isozymes, and meprin activity [23].
• The H-2L locus is closely linked to H-2D and codes for antigenic specificities present on a 45,000 mol wt glycoprotein that is distinct from the molecule which bears the D region private specificity [24].
• Adsorption experiments showed that the only cells capable of adsorbing the suppressor factor are DNFB-immune T cells from donors which share with the factor-producing strain either the H-2K or H-2D locus [25].
• Dimethyl sulfoxide (DMSO) has previously been shown to increase the surface expression of H-2K and H-2D antigens on cultured line 1 carcinoma cells [26].
• In the present study, a number of B10 congenic and recombinant mouse strains were investigated to determine the H-2K and H-2D-restricted FTC-self CTL response patterns, and these were compared with the CTL response patterns obtained for TNP-self [27].

Physical interactions of H2-D1

• With the s haplotype the rosetting receptor was mapped to the H-2L/H-2D region, whereas with the b and q haplotypes rosetting was only mapped to the D end of the H-2 complex [28].

Regulatory relationships of H2-D1

• These spleen cells displayed strong lysis on TNP-modified H-2D end-matched (Kd-Dk) targets as well as enhanced cytotoxicity against H-2 matched (Kk-Dk) or H-2K end-matched (Kk-Dd) target cells [29].
• AKR leukemia cell lines differing in the amount of H-2K and H-2D antigens expressed on the cell surface were used to assess cell-mediated immune responses in syngeneic mice against Gross/AKR murine leukemia virus (MuLV)-induced tumors [30].

Other interactions of H2-D1

• The finding that the D region controls H-2L and H-2M, as well as H-2D, molecules suggests that the system of H-2 antigens is more complicated [31].
• The restriction of the response to the H-3 antigen requires effector-target identity of the H-2D molecule but not the B2M molecule of the class I antigen [32].
• We have defined the genetic locus responsible for ultraviolet B susceptibility and resistance in mice within the Bat5 and H-2D segment of the mouse chromosome 17 [33].
• These results suggest that there is a mechanism that regulates, at the transcriptional level, the coordinate expression of H-2K and H-2D heavy chains, and the beta 2m light chains encoded by genes on chromosomes 17 and 2, respectively [3].
• Proximity of the Mep-1 gene to H-2D on chromosome 17 in mice [23].

Analytical, diagnostic and therapeutic context of H2-D1

• The mouse major transplantation antigens H-2K, H-2D and H-2L are highly polymorphic cell-surface glycoproteins which may serve as recognition elements in cell-cell interactions [34].
• OBJECTIVES: The polymerase chain reaction (PCR)-based method was used to obtain and sequence three H-2K and three H-2D mouse complementary DNAs (cDNA) of class I major histocompatibility complex (MHC) molecules [35].
• Sequence analysis has revealed that class I genes from the H-2D subregion of the MHC (which includes the D and L genes) differ from the class I gene from the H-2K subregion (the K gene) by the insertion of a type 2 Alu-like repetitive element (the murine B2 sequence) within the 3' noncoding region of the D and L genes [36].
• To check whether the H-2D-linked loci are solely responsible for the fate of bone marrow allografts, we measured the strength of resistance of irradiated (B6 X C3H)F1 and (B6 X BALB/c)F1 recipients toward bone marrow grafts from a set of H-2 recombinant and F1 hybrid donors carrying either the H-2b, H-2d, and H-2k alleles [37].
• The adoptive transfer of DTH is restricted to H-2K or H-2D compatible donor-recipient combinations [38].

References