Abstract
Recent advances in deciphering the genetic architecture of RA-ILD support the hypothesis of RA-ILD as a complex disease with a heterogeneous phenotype encompassing at least the usual interstitial pneumonia (UIP) and non-UIP high-resolution CT patterns. The results of genetic studies support the hypothesis of a common genetic background between idiopathic pulmonary fibrosis (IPF) and RA-ILD, and more specifically RA-UIP, a subset of the disease associated with a poor prognosis. Overall, these findings suggest the existence of shared pathogenic pathways between IPF and RA-ILD providing new opportunities for future intervention in RA-ILD, particularly with drugs that have been shown to be active in IPF.
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