Molecular immunogenetics in susceptibility to bovine dermatophilosis: a candidate gene approach and a concrete field application

To identify molecular genetic markers of resistance or susceptibility to dermatophilosis in cattle, we used a functional candidate gene approach to analyze the DNA polymorphisms of targeted genes encoding molecules implicated in known mechanisms of both nonspecific and specific immune responses exis...

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Veröffentlicht in:Annals of the New York Academy of Sciences 2002-10, Vol.969 (1), p.92-96
Hauptverfasser: Maillard, Jean-Charles, Chantal, Isabelle, Berthier, David, Thevenon, Sophie, Sidibe, Issa, Razafindraibe, Hanta
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Sprache:eng
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Zusammenfassung:To identify molecular genetic markers of resistance or susceptibility to dermatophilosis in cattle, we used a functional candidate gene approach to analyze the DNA polymorphisms of targeted genes encoding molecules implicated in known mechanisms of both nonspecific and specific immune responses existing in the pathogen/host interface mechanisms. The most significant results were obtained within the Major Histocompatibility Complex (MHC) where the BoLA-DRB3 and DQB genes encode molecules involved in the antigen presentation to T cell receptors. A unique BoLA class II haplotype, made up of one DRB3 exon 2 allele and one DQB allele, highly correlates with the susceptibility character (P < 0.001). This haplotype marker of susceptibility was also found and validated in other bovine populations. A eugenic marker-assisted selection was developed in the field by eliminating only the animals having this haplotype. The disease prevalence was thereby reduced from 0.76 to 0.02 over 5 years. A crossbreeding plan is in progress to study the genetic transmission of the genotypic and phenotypic characters of susceptibility to dermatophilosis. In conclusion, we discuss several hypotheses at the molecular and cellular levels to better define the exact role of the MHC molecules in disease control and to answer the question: How is MHC diversity selectively maintained by natural selection imposed by pathogens?
ISSN:0077-8923
1749-6632
DOI:10.1111/j.1749-6632.2002.tb04357.x