Molecular analyses confirm similar inflammation in CR and AD compared with HCs. (A) CD14⁺ HLA-DR^low monocytes and activated (HLA-DR⁺) T cells were sorted from fresh peripheral blood PBMCs for bulk RNA sequencing. (B) The transcription profile of activated (HLA-DR⁺) T cells of CR DLBCL was compared with those from patients with AD and HCs in an unsupervised clustering. (C) Pathway analysis of the significantly differentially expressed genes of activated (HLA-DR⁺) T cells highlights signature 1 with reduction of mitochondrial respiration and electron transport in AD and CR compared with HCs. Changes of gene expression levels were determined by Z values. (D) Transcription profiles of CD14⁺/HLA-DR^low monocytes from HCs and patients in CR or with AD were unsupervised clustered. (E) CR samples from panel D were manually annotated to either HC-like CR or AD-like CR and unsupervised clustering repeated with the 4 distinct subgroups. (F) Exemplary signature of the 4-group analysis with upregulation of the IFN-α/β signature. Changes of gene expression levels were determined by Z values. (G) Visualizing of the patients HC- and AD-like profiles in the previously shown immunophenotypic pattern PCA from Figure 2H. (H) Cytokine profile of 92 cytokines Olink analysis from serum of patients in CR was clustered by K-means in 2 subgroups by the Elbow method. HC- (green circle) and AD-like samples (blue circles) from the RNA sequencing are indicated. (I) The differentially expressed cytokines of cluster 1 were subtracted by cluster 2 and plotted against their significance levels given by the logarithm of the adjusted P value, that is, −log₁₀ (adj.p). AD., active disease; Dim., dimension; fig., figure; HLA-DR., human leukocyte antigen type DR; IFNa/b, interferon alpha or beta; IL-6, interleukin-6; TNF, tumor necrosis factor.