Genome-wide mapping of gene–microbiota interactions in susceptibility to autoimmune skin blistering

摘要: Susceptibility to chronic inflammatory diseases is determined by immunogenetic and environmental risk factors. Resident microbial communities often differ between healthy diseased states, but whether these differences are of primary aetiological importance or secondary the altered environment remains largely unknown. Here we provide evidence for host gene–microbiota interactions contributing disease in a mouse model epidermolysis bullosa acquisita, an autoantibody-induced skin disease. Using advanced intercross, identify genetic loci microbiota variability, susceptibility blistering their overlap. Furthermore, treating bacterial species abundances as covariates with reveal novel locus. The majority identified covariate taxa characterized reduced abundance being associated increased risk, providing role protection from Further characterization putative probiotic assemblages offers promising potential preventative therapeutic treatment development.