IL-23 favours outgrowth of spondyloarthritis-associated pathobionts and suppresses host support for homeostatic microbiota.

Linda M RehaumeNicholas MatigianAhmed M MehdiNancy LachnerKate L BowermanJoshua DalyKim-Anh Lê CaoPhilip HugenholtzRanjeny Thomas

Published in: Annals of the rheumatic diseases (2019)

Dysbiosis in SKG mice reflects human SpA and is IL-23p19 dependent. In genetically susceptible hosts, IL-23p19 favours outgrowth of SpA-associated pathobionts and reduces support for homeostatic-inducing microbiota. The relative abundance of specific pathobionts is associated with disease severity.

Keyphrases

endothelial cells
signaling pathway
type diabetes
metabolic syndrome
induced pluripotent stem cells
high fat diet induced
systemic lupus erythematosus
insulin resistance
microbial community