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Poster Session

Rheumatoid Arthritis (RA)

Poster Session C

Session: (2265ā€“2289) Rheumatoid Arthritis ā€“ Treatment Poster III

2277: Immunophenotyping of peripheral blood mononuclear cells reveals potential cellular biomarkers of disease in rheumatoid arthritis

Tuesday, October 28, 2025
10:30 AM - 12:30 PM Central Time
Location: Hall F1

    Abstract Poster Presenter(s)

  • JB

    John Bui, BSc

    Sonoma Biotherapeutics
    Seattle, Washington, United States

    Disclosure(s): Bristol-Myers Squibb(BMS): Equity interest (Ongoing)


Background/Purpose: Emerging cell-based therapies for rheumatoid arthritis (RA) target the underlying immunologic activity of disease. Objective biomarkers to-date are downstream sequelae of RA immunologic drivers. In this study, we sought to identify direct cellular biomarkers in RA by comprehensively profiling immune subsets from whole blood.

Methods: Here, three flow cytometry panels measuring 18 markers were used to identify T cell subsets. PBMC were profiled from 30 RA subjects with varying disease severity measured by DAS28-CRP, DAS28-ESR and CDAI in addition to 23 age-, gender-, and race-matched healthy donor control subjects (HD). A two-tiered approach was applied for data analysis: Tier 1) Identify cell subsets significantly different between RA and HD and Tier 2) Correlate cell subsets identified in Tier 1 with RA clinical disease severity.

Results: The analysis revealed a significant difference (pā‰¤0.001) between RA (12%) and HD (39%) in the frequency of an effector regulatory T cells (Treg) phenotype defined by CD4+FOXP3+CD25hiCD45RA-. Furthermore, the frequency of these cells was inversely correlated with disease severity measured by DAS28-CRP (r = -0.525, p = 0.039). Activation and proliferation markers on the Tregs in the RA subjects were similarly inversely correlated with DAS28-CRP (r= -0.53 HLA-DR, r= -0.49 CTLA-4, r= -0.52 Ki67). In contrast, the T effector cell subset phenotype data reveal significantly higher frequency (p=0.001) of CD4+CD45RA-CCR7+ central memory CD4+ T cells (Tcm) in RA (31%) compared to HD (20%). Moreover, the frequency of CD4+ Tcm was positively correlated with DAS28-ESR (r = 0.615, p = 0.037).

Conclusion: We show that, compared to healthy subjects, RA patients have significantly reduced proportion of Tregs with an effector phenotype and a higher proportion of CD4 Tcm. These phenotypic frequencies correlate with disease severity, highlighting a relationship of these immune subsets to the pathogenesis of RA. Additional characterization of these subsets will be pursued to determine their potential utility as pharmacodynamic biomarkers.