A disease-associated gene desert directs macrophage inflammation through ETS2.

ABSTRACT: Increasing rates of autoimmune and inflammatory disease present a burgeoning threat to human health¹. This is compounded by the limited efficacy of available treatments¹ and high failure rates during drug development², highlighting an urgent need to better understand disease mechanisms. Here we show how functional genomics could address this challenge. By investigating an intergenic haplotype on chr21q22-which has been independently linked to inflammatory bowel disease, ankylosing spondylitis, primary sclerosing cholangitis and Takayasu's arteritis^3-6-we identify that the causal gene, ETS2, is a central regulator of human inflammatory macrophages and delineate the shared disease mechanism that amplifies ETS2 expression. Genes regulated by ETS2 we

SUBMITTER: Stankey CT 

PROVIDER: S-EPMC11168933 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature