GM-CSF Expression and Macrophage Polarization in Joints of Undifferentiated Arthritis Patients Evolving to Rheumatoid Arthritis or Psoriatic Arthritis

Background and Aims GM-CSF-dependent macrophage polarization has been demonstrated in rheumatoid arthritis (RA). Our aim was to seek diagnostic/prognostic biomarkers for undifferentiated (UA) by analyzing GM-CSF expression source, density joints of patients with UA evolving RA or PsA compared established PsA, respectively. Methods Synovial tissue (ST) from (UA>RA, n=8), (UA>PsA, n=9), persistent (UA, n=16), (n=12) (n=10), healthy controls (n=6), were analyzed. Cell source quantitative proteins associated pro-inflammatory (GM-CSF-driven) anti-inflammatory (M-CSF-driven) (activin A, TNFα, MMP12, CD209, respectively) assessed ST CD163 + macrophages multicolor immunofluorescence. activin A levels also quantified paired synovial fluid samples. determined all groups Results stromal cells (FAP CD90 fibroblast, endothelial cells) sublining the sources GM-CSF. expressed markers MMP12). Expression M-CSF-dependent marker CD209 identified two subsets (CD163 high low/- ). more abundant patients, although both subtypes showed similar groups. In samples, detected higher UA>RA RA, while infrequently detected. comparable between UA>PsA but significantly than UA. Conclusions is highly FAP fibroblasts, activated endothelium different types arthritis. The state groups, a predominance GM-CSF-associated markers. phases Taken together, our findings support idea that strong driver potential therapeutic target not only