Whole blood gene expression of rheumatoid arthritis. Homo sapiens

Sustained clinical remission (CR) without drug treatment has not been achieved in patients with rheumatoid arthritis (RA). This implies a substantial difference between CR and the healthy state, but it has yet to be quantified. We report a longitudinal monitoring of the drug response at multi-omics levels in the peripheral blood of patients with RA. Our data reveal that drug treatments alter the molecular profile closer to that of HCs at the transcriptome, serum proteome and immunophenotype level. Patient follow-up suggests that the molecular profile after drug treatments is associated with long-term stable CR. In addition, we identify molecular signatures that are resistant to drug treatments. These signatures are associated with RA independently of known disease severity indexes and are largely explained by the imbalance of neutrophils, monocytes, and lymphocytes. This high-dimensional phenotyping provides a quantitative measure of molecular remission and illustrates a multi-omics approach to understanding drug response. Overall design: Transcriptome of whole blood from RA patients with or without drug treatments (methotrexate, infliximab, and tocilizumab) and healthy volunteers. Serum proteins measured by SOMAscan and peripheral immune cell counts were also measured for the same blood samples and can be found at http://dx.doi.org/10.7303/syn8483403 .