scholarly journals A tangled history: patterns of major histocompatibility complex evolution in the African mole-rats (Family: Bathyergidae)

2007 ◽  
Vol 91 (3) ◽  
pp. 493-503 ◽  
Author(s):  
SAMIT KUNDU ◽  
CHRISTOPHER G. FAULKES
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Major Histocompatibility Complex Evolution

scholarly journals Forces shaping major histocompatibility complex evolution in two hyena species

2013 ◽  
Vol 94 (2) ◽  
pp. 282-294 ◽  
Author(s):  
Katy J. Califf ◽  
Elizabeth K. Ratzloff ◽  
Aaron P. Wagner ◽  
Kay E. Holekamp ◽  
Barry L. Williams
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Major Histocompatibility Complex Evolution

scholarly journals Adaptive tolerance to a pathogenic fungus drives major histocompatibility complex evolution in natural amphibian populations

2016 ◽  
Vol 283 (1827) ◽  
pp. 20153115 ◽  
Author(s):  
Anna E. Savage ◽  
Kelly R. Zamudio
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Batrachochytrium Dendrobatidis ◽  
Pathogenic Fungus ◽  
Natural Populations ◽  
Major Histocompatibility ◽  
Evolutionary Potential ◽  
Histocompatibility Complex ◽  
Molecular Signal ◽  
Major Histocompatibility Complex Evolution

Amphibians have been affected globally by the disease chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis ( Bd ), and we are just now beginning to understand how immunogenetic variability contributes to disease susceptibility. Lineages of an expressed major histocompatibility complex (MHC) class II locus involved in acquired immunity are associated with chytridiomycosis susceptibility in controlled laboratory challenge assays. Here, we extend these findings to natural populations that vary both in exposure and response to Bd . We find that MHC alleles and supertypes associated with Bd survival in the field show a molecular signal of positive selection, while those associated with susceptibility do not, supporting the hypothesis that heritable Bd tolerance is rapidly evolving. We compare MHC supertypes to neutral loci to demonstrate where selection versus demography is shaping MHC variability. One population with Bd tolerance in nature shows a significant signal of directional selection for the same allele (allele Q) that was significantly associated with survival in an earlier laboratory study. Our findings indicate that selective pressure for Bd survival drives rapid immunogenetic adaptation in some natural populations, despite differences in environment and demography. Our field-based analysis of immunogenetic variation confirms that natural amphibian populations have the evolutionary potential to adapt to chytridiomycosis.

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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