Monocyte-derived transcriptomes explain the ineffectiveness of abatacept in rheumatoid arthritis
Authors' conclusion
Monocyte-derived transcriptomic features before treatment underlie the differences in abatacept efficacy in patients with RA.
Study context
- Population
- Rheumatoid arthritis (RA) patients treated with abatacept; blood samples at baseline and after 3 monthsreplication: 27 responders, 50 non-responders
- Participants
- 22 patients
- Comparison
- Abatacept responders vs non-responders
- Respondersn = 7reference
- Outcome
- Cellular, transcriptomic and proteomic features predicting resistance to abatacept
Methodological detailsreplication in three gene expression data sets
- Replication in three gene expression data sets
Main finding
As reported in the abstract
- Number of monocytes significantly higher in non-responders before treatment
- Differentially expressed genes (DEGs) between responders and non-responders enriched in monocytes
- TLR5 and IL17RA pathway in monocytes upregulated in non-responders
- Hepatocyte growth factor (HGF), correlated with this signature, higher in non-responders before treatment
Further findings
Replication set (three gene expression data sets)
- DEGs enriched for monocyte-expressed genes, not for TLR5 and IL17RA pathway but for oxidative phosphorylation (OXPHOS) pathway
Original publication
Monocyte-derived transcriptomes explain the ineffectiveness of abatacept in rheumatoid arthritis. Arthritis Res Ther. Published 2 January 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →