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[Preprint]. 2024 Nov 12:2024.10.25.620344. [Version 2] doi: 10.1101/2024.10.25.620344

Fig. 2: Longitudinal changes in naive and CM CD4 T cells dominate progression to clinical RA.

Fig. 2:

(A) Overview of longitudinal comparison of converters, from ‘at-risk’ to clinical RA. (B) Number of genes per Allen Institute for Immunology level 2 cell type with higher average intra-donor coefficients of variation (CVs) over time in ARI who progress to clinical RA (orange) or in CON2 (green). (C) Comparison of the number of differentially expressed genes (DEGs) (y-axis) with the change in frequency over time (x-axis; centered log-ratio (CLR) transformed) as ARI progress to clinical RA. Bubble size corresponds to the aggregate score calculated by [-log(padj CLR frequency changes) x total number of DEGs]. (D) Number of DEGs from longitudinal model (FDR<0.1) per level 3 immune cell type, elevated (above 0) or diminished (below 0) in ARI progressing to clinical RA. (E-I) Overview (E) of paired comparison in converters at their last ‘at-risk’ pre-symptomatic visit vs. time of their clinical RA diagnosis. (F) Normalized RNA expression of TNF in Core CD16 monocytes and CXCL10 in ISG+ CD16 monocytes. (G) Mean RNA expression of select inflammatory genes amongst monocyte level 3 cell types. (H) Gene scores calculated by comparing marker genes from FOLR2+ICAM+ RA synovial tissue macrophages (Alivernini 2020) among all monocyte cell types. (I) Frequency of IL1B+ CD14 monocytes within CD14 monocytes. Effect sizes and P values were determined by linear mixed effect models (C,D), paired Wald test (F), or paired Wilcoxon test (I). FDR values are indicated for all panels.