Major histocompatibility complex variation and the evolution of resistance to amphibian chytridiomycosis

Major histocompatibility complex variation and the evolution of resistance to amphibian... Chytridiomycosis, caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd), has been implicated in population declines and species extinctions of amphibians around the world. Susceptibility to the disease varies both within and among species, most likely attributable to heritable immunogenetic variation. Analyses of transcriptional expression in hosts following their infection by Bd reveal complex responses. Species resistant to Bd generally show evidence of stronger innate and adaptive immune system responses. Major histocompatibility complex (MHC) class I and class II genes of some susceptible species are up-regulated following host infection by Bd, but resistant species show no comparable changes in transcriptional expression. Bd-resistant species share similar pocket conformations within the MHC-II antigen-binding groove. Among susceptible species, survivors of epizootics bear alleles encoding these conformations. Individuals with homozygous resistance alleles appear to benefit by enhanced resistance, especially in environmental conditions that promote pathogen virulence. Subjects that are repeatedly infected and subsequently cleared of Bd can develop an acquired immune response to the pathogen. Strong directional selection for MHC alleles that encode resistance to Bd may deplete genetic variation necessary to respond to other pathogens. Resistance to chytridiomycosis incurs life-history costs that require further study. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Immunogenetics Springer Journals

Major histocompatibility complex variation and the evolution of resistance to amphibian chytridiomycosis

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag Berlin Heidelberg
Subject
Biomedicine; Immunology; Human Genetics; Gene Function; Cell Biology; Allergology
ISSN
0093-7711
eISSN
1432-1211
D.O.I.
10.1007/s00251-017-1008-4
Publisher site
See Article on Publisher Site

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