Participation of the Major Histocompatibility Complex in the Determination of Familial Malignancies1

2015 ◽  
pp. 213-221
Author(s):  
J. Hors ◽  
J. Gony ◽  
J. M. Andrieu ◽  
J. P. Cesarini ◽  
F. Teillet ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

scholarly journals Determination of a Predictive Cleavage Motif for Eluted Major Histocompatibility Complex Class II Ligands

2018 ◽  
Vol 9 ◽  
Author(s):  
Sinu Paul ◽  
Edita Karosiene ◽  
Sandeep Kumar Dhanda ◽  
Vanessa Jurtz ◽  
Lindy Edwards ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Cleavage Motif

GLUCOCORTICOID-INDUCED CLEFT PALATE IN THE MOUSE: TWO MAJOR HISTOCOMPATIBILITY COMPLEX, H-2, LOCI WITH DIFFERENT MECHANISMS

Genetics ◽  
1983 ◽  
Vol 103 (2) ◽  
pp. 263-276
Author(s):  
Joseph J Bonner ◽  
Marvin L Tyan
Keyword(s):  
Major Histocompatibility Complex ◽  
Cleft Palate ◽  
Inbred Strains ◽  
Response Analysis ◽  
Major Histocompatibility ◽  
Factors Affecting ◽  
Histocompatibility Complex ◽  
Pregnant Mice ◽  
Isolated Cleft Palate

ABSTRACT Isolated cleft palate is induced in the progeny of pregnant mice that are given glucocorticoids. The incidence varies among inbred strains and with dose and stage of gestation when the drug is given. One chromosomal region responsible for strain-associated differences in sensitivity is the major histocompatibility complex, H-2. H-2a is associated with susceptibility, H-2b with resistance. There appear to be both maternal and embryonic genetic factors affecting the sensitivity to glucocorticoids. In experiments reported here congenic strains of mice with H-2a, H-2d and H-2k haplotypes on a C57BL/10 genomic background were used. This allowed the determination of the effect on sensitivity by two H-2 subregions; the subregions are H-2K to I-E and I-C to H-2D. Methods included dose-response analysis and reciprocal cross analysis using dexamethasone given on day 12 of pregnancy. Results show that each subregion affects the strain's sensitivity to dexamethasone-induced cleft palate. The regression coefficients for B10.A-H-2a (45.4 ± 4.13) were different from those for B10.BR-H-2k (67.2 ± 10.8) and B10.D2-H-2d (70.5 ± 9.74). The estimated mean arcsine% cleft palate at 160 mg/kg was different for each strain: B10.A-H-2a, 53.1 ± 2.19; B10.BR-H-2k, 33.1 ± 2.27; B10.D2-H-2d, 25.0 ± 2.75. Different patterns of change in sensitivity were observed among the reciprocal crosses. In summary, the H-2K to I-E subregion seemed to influence both maternal and embryonic factors, whereas only embryonic factors were influenced by the I-C to H-2D subregion. These data suggest that the mechanisms affecting glucocorticoid sensitivity which are genetically encoded within each H-2 subregion are different, and there is an interaction between the alleles. The mode of interaction can be either complementation or epistasis.

Determination of a major histocompatibility complex class I restricting simian immunodeficiency virus Gag241???249 epitope

AIDS ◽  
2008 ◽  
Vol 22 (8) ◽  
pp. 993-994 ◽  
Author(s):  
Tetsuo Tsukamoto ◽  
Sachi Dohki ◽  
Takamasa Ueno ◽  
Miki Kawada ◽  
Akiko Takeda ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Simian Immunodeficiency Virus ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Immunodeficiency Virus

Major Histocompatibility Complex Class I-related Chains A and B (MIC A/B): A Role in the Pathogenesis of Non-alcoholic Steatohepatitis

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
A Kahraman ◽  
S Menziletoglu Yildiz ◽  
M Schlattjan ◽  
A Kilicarslan ◽  
CD Fingas ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Alcoholic Steatohepatitis ◽  
Histocompatibility Complex

Relationship of Major Histocompatibility Complex Class II Genes to Inhibitor Antibody Formation in Hemophilia A

1990 ◽  
Vol 64 (04) ◽  
pp. 564-568 ◽  
Author(s):  
Lloyd E Lippert ◽  
Lyman Mc A Fisher ◽  
Lawrence B Schook
Keyword(s):  
Major Histocompatibility Complex ◽  
Factor Viii ◽  
Antibody Formation ◽  
Rflp Analysis ◽  
Class Ii ◽  
Major Histocompatibility ◽  
Odds Ratios ◽  
Inhibitory Antibody ◽  
Histocompatibility Complex ◽  
Hla Dr

SummaryApproximately 14% of transfused hemophiliacs develop an anti-factor VIII inhibitory antibody which specifically neutralizes factor VIII procoagulant activity. In this study an association of the major histocompatibility complex (MHC) with inhibitor antibody formation was evaluated by restriction fragment length polymorphism (RFLP) analysis using BamHI, EcoRI, HindII, PstI, PvuII and TaqI digested genomic DNA probed with DP beta, DQ alpha, DQ beta and DR beta class II MHC gene probes. The RFLP patterns for 16 non-inhibitor and 11 inhibitor hemophiliac patients were analyzed. These 24 enzyme:probe combinations generated 231 fragments. Fifteen (15) fragments associated with the inhibitor phenotype; odds ratios ranged from 5.1 to 45 and lower bounds of 95% confidence intervals were > 1.000 for all 15 fragments. Five (5) fragments associated with non-inhibitors, with odds ratios ranging from 6.4 to 51.7. This report establishes a MHC related genetic basis for the inhibitor phenotype. No statistically significant differences in the distribution of serologically defined HLA-DR phenotypes were observed between the inhibitor and non-inhibitor groups.

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