Persisting systemic inflammation in CR is distinct from AD. (A) Serum levels of soluble CD25 (sCD25), CXCL9, and CXCL10 or (B) of proinflammatory IL-6, beta-2-microglobuline (B2M), and soluble CD14 (sCD14) were determined from serum samples of HCs and patients in CR, ND patients or patients with R/R disease by enzyme-linked immunosorbent assay. Each symbol indicates individual patients, P values were determined by ANOVA including 2-group comparison using the Šidák multiple comparison when indicated. (C) Serum IL-6 concentration was correlated with absolute M-MDSCs per μL from the peripheral blood of patients in CR, R2 of matching is indicated. (D) Monocytes of HCs were differentiated using GM-CSF with or without IL-6 in vitro, and rate of HLA-DRlow monocytes was determined by flow cytometry. Each symbol represents an individual HC, P values were determined by the matched-pair ordinary ANOVA. (E) Absolute counts of CD4+ Tn cells were correlated with serum levels of IL-6. (F) Cytokine profiles of 72 patients with DLBCL in relapse were compared with profiles of 43 patients with DLBCL in remission to assess the different inflammation profile between the 2 groups. Each circle corresponds to an individual patient with R/R disease (blue) or CR (red). (G) Volcano plot showing the fold change and significance level of significantly upregulated or downregulated serum cytokines in R/R compared with CR. For all panels, ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. adj., adjusted; CXCL, C-X-C motif chemokine ligand; FASLG, fas ligand; GM-CSF, granulocyte-macrophage colony-stimulating factor; ns, not significant; OX40, TNF receptor superfamily member 4; Stim., stimulated; Tn, naive T cells; TRAIL, tumor necrosis factor-related apoptosis-inducing ligand.