Disease relevance of H2

• Inbred and congeneic strains of mice have been examined for susceptibility to cortisone-induced cleft palate, and the role of genes linked to H-2 on chromosome 17 has been confirmed [1].
• The L1210 leukemia cell bears a B lymphocyte specific, non-H-2 linked alloantigen [2].
• Susceptibility to glomerulonephritis was linked to H2 (Chr 17, LOD = 2.37 - 2.70), Swrl-2 (Chr 14, 36 cM, LOD = 2.48 - 2.71), and Nba1 (Chr 4, 75 cM, LOD = 2.15 - 2.23) [3].
• New revelations in susceptibility to autoimmune thyroiditis by the use of H2 and HLA class II transgenic models [4].
• Absence of significant H-2 and beta 2-microglobulin mRNA expression by mouse embryonal carcinoma cells [5].

Psychiatry related information on H2

• This finding is most readily accommodated within the altered self concept (postulating that T cells are specific for virus-modified self structures) but cannot exclude the possibility of a physiological interaction mechanism being responsible for the apparent H-2 restriction of virus-specific cytotoxic T cells [6].

High impact information on H2

• The H-2 genes encode ubiquitously expressed transplantation antigens that serve as recognition structures for cytotoxic T cells [7].
• A panel of target cells was obtained by the double transfection and expression of a retrovirus gene and a foreign H-2 gene in recipient mouse fibroblasts [8].
• They display enhancer-like activity in cells that express H-2 genes, but show some tissue specificity in that they function very poorly in undifferentiated embryonal carcinoma cells in which H-2 genes are not expressed [9].
• On genomic DNA blots, the restriction fragments containing H-2-related sequences were highly variable among different inbred strains of mice, whereas they were very similar among different t haplotypes even when the t haplotypes carried serologically different H-2 haplotypes [10].
• Naturally occurring t haplotypes suppress recombination over a region of mouse chromosome 17 that includes the H-2 complex [11].

Chemical compound and disease context of H2

• Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes [12].
• We have constructed two hybrid plasmids containing the 5' flanking region of an H-2Kb gene followed by the coding regions of either the herpes simplex virus thymidine kinase (H-2 tk) or the chloramphenicol acetyl transferase (H-2 CAT) genes [13].
• We have reported that susceptibility to glucocorticoid- and phenytoin-induced cleft palate and glucocorticoid receptor levels in mice are influenced by the H-2 histocompatibility complex on chromosome 17 [14].
• Susceptibility to Bordetella pertussis-induced sensitivity to serotonin was found to be associated with the H-2 gene complex in mice [15].
• However, some of the strains of mice with the same H-2 haplotype but otherwise different genetic backgrounds had different responses to bleomycin, suggesting that there is also a role for non-H-2 genetic factors in modulating the response to this experimental interstitial lung disease [16].

Biological context of H2

• A linkage study showed that Glo-1 maps at approximately 3 centimorgans from the Ss locus of the H-2 histocompatibility region [17].
• Given the broad expression of H-2 class Ib molecules on hematopoietic cells, antigen presentation pathways among CD1d expressing cells might tightly regulate CD1d-restricted natural killer T (NKT) cells [18].
• It appeared that the H-2aw18 haplotype has a single, recessive, lethal mutation, since homozygotes for H-2aw18 were not detected in progeny generated from the intercross of mice that were heterozygous for this H-2 haplotype [19].
• Nine newly established recombinant H-2 haplotypes, which arose from the heterozygous mice that resulted from a cross between common inbred H-2 haplotypes and the aw18 haplotype, allowed us to map the lethal gene to the class III region of the H-2 complex [19].
• Murine complement component 3: genetic variation and linkage to H-2 [20].

Anatomical context of H2

• In conclusion, our results demonstrate that both H1 and H2 receptors are involved in learning and memory processes for which the frontal cortex, amygdala and hippocampus interact [21].
• Transformation of murine NIH3T3 fibroblasts with retroviral vectors carrying the mos, myc and the Ha-ras oncogene, respectively, was associated with a strong reduction of H2 antigen expression in the cell membrane [22].
• The K and D regions of the H-2 gene complex are highly polymorphic and control cell-surface structures involved in the H-2 restriction of cytotoxic T lymphocytes [23].
• Comparison of H-2 antigens immunoprecipitated from normal spleen cells and from thioglycollate-induced adherent peritoneal exudate cells cultured in the presence or absence of supernatant fluids from concanavalin A-stimulated spleen cells revealed that H-2K' was not expressed on the adherent peritoneal cells [24].
• V beta 3+ T cells are eliminated in Mls-2a mice carrying some, but not all, H-2 types [25].

Associations of H2 with chemical compounds

• Selective cognitive dysfunction in mice lacking histamine H1 and H2 receptors [21].
• Glyoxalase I polymorphism in the mouse: a new genetic marker linked to H-2 [17].
• Lethal deletion of the complement component C4 and steroid 21-hydroxylase genes in the mouse H-2 class III region, caused by meiotic recombination [19].
• We have continued our investigations of line lung carcinoma cells to understand the molecular basis of decreased expression of class I H-2 Ag and class I Ag induction with DMSO [26].
• Sgp-1b, which appeared in most of the H-2 types tested, corresponds with low serum gp70 output in B10 congenic lines and F1 hybrid offspring of B10 and NZB crosses and with increased gp70 production after lipopolysaccharide (LPS) stimulation [27].

Physical interactions of H2

• The results indicated that murine Bf was controlled by a single codominant locus located close to the H-2 complex because no mouse showing recombination between Bf locus and S locus was found [28].
• We include into the H-2 complex the cluster of Qa and Tla loci, which we consider as class I loci (Klein et al. 1983) [29].
• The most straightforward interpretation of the results presented here is that these t haplotypes carry an H-2 complex located between the centromere and tufted locus [30].
• Chromosome 17 of the mouse carries the H-2 complex and the T/t complex [31].
• Linkage studies showed that both of the major NZB and NZW genes are loosely linked to the H-2 complex but not to either the Mup-1 or coat color gene loci examined [32].

Regulatory relationships of H2

• First, a profound inhibition of primary PFC responses occurs when foreign H-2 antigens are expressed on Thy-1 incompatible donor cells [33].
• Our results demonstrate that the Ity gene may modulate the antibody responses to the foreign antigen but that the major genetic influence is exerted by H-2 genes, which control the capacity of mice to respond to the antigen expressed by recombinant attenuated Salmonella cells [34].
• These experiments suggest that alloantisera to the H-2 complex express at least part of their inhibitory properties by blocking the Fc receptor on B cells, and the data support the concept that certain Ia antigens and the Fc receptor are identical or closely associated [35].
• These findings suggest the possibility that orexin A may activate H1 and H2 receptors in the supraspinal levels through the release of histamine from neurons, which might attenuate the antinociceptive effects of orexin A [36].

Other interactions of H2

• 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 [23].
• In three such crosses, with 5* offspring, C3 segregated with H-2 in 46 instances, corresponding to a recombination frequency of approximately equal to 0.12 [20].
• Control of H-2 class I and beta 2-microglobulin gene expression by M-MuLV, and probably by M-MSV, takes place at the transcriptional level as indicated by nuclear runoff studies and analysis of steady-state mRNA levels [37].
• Evidence for placing the Neu-1 locus within the mouse H-2 complex [38].
• A classical breeding analysis of the complete t haplotypes, tw5 and t12, utilizing the newly induced markers, reveals two inversions in t chromatin: one involving T and qk, and one involving tf and the H-2 complex [39].

Analytical, diagnostic and therapeutic context of H2

• A gene mapping between the S and D regions of the H-2 complex influences resistance to Trichinella spiralis infections of mice [40].
• In L cells, these genes direct the synthesis of hybrid H-2 proteins and by using monoclonal antibodies of defined specificities, we have mapped classically defined serological specificities to structurally defined domains of the transplantation antigen protein [41].
• Sequence analysis of mouse H-2 cDNA clones has suggested the existence of an unusual class of H-2 (class I)-related antigens that, unlike the classical membrane-associated molecules, retains only the extracellular portion and is likely to be secreted [42].
• Qa-1-specific, H-2-unrestricted cytotoxic T lymphocytes (CTLs) generated from reciprocally immunized B10.BR (H-2k, Qa-1a) and CBA (H-2k, Qa-1b) mice, and immunoprecipitation of cell surface Qa-1 were used to examined Qa-1 region determinant expression by H-2r and H-2f mice [43].
• We have found the definitive location of the H-2 complex by the use of in situ hybridization [31].

References