Fig 1: Translating omics-based classification of MPA to the bedside.a Serum IFN-α concentrations and the percentage of monocytes among PBMCs in the complete blood count of samples from patients with MPA (n = 43). The 10 samples with the highest percentage of monocytes were classified as MPA-MONO (pink colored dots). The 10 samples with the highest IFN-α concentrations were classified as MPA-IFN (green colored dots). b Characteristic symptoms of patients in the MPA-MONO (n = 9) and MPA-IFN (n = 9) groups. Scores for each component are based on the Birmingham Vasculitis Activity Score (BVAS) 2008 version 3. Mucous; Mucous membranes, ENT; Eyes, nose, and throat. c Annualized relapse rate of patients in the MPA-MONO (n = 9) and MPA-IFN (n = 9) groups. Symptoms at relapse are displayed for each case based on the components of the BVAS. “Nvs” refers to the nervous system. d Correlation between the percentage of monocytes and representative clinical parameters, and between serum IFN-α concentrations and representative clinical parameters. Correlations and P-values were quantified using Kendall’s correlation coefficient (R). CRP C-reactive protein, MPO myeloperoxidase, ANCA anti-neutrophil cytoplasmic antibody. e Differences in serum IFN-α concentrations and monocyte ratio in patients with newly-onset cases (n = 30) and cases under treatment (n = 13). f Receiver Operating Characteristic (ROC) curve for predicting relapse of MPA from serum IFN-α concentration and percentage of monocytes in PBMCs. Values are means with SEMs and P-values are calculated using a two-sided Mann–Whitney U test for b, c, and e. Source data are provided as a Source Data file.
Fig 2: Graphical scheme of this study.Newly-onset, untreated patients with MPA (n = 8) and healthy donors (n = 7) were recruited for this study. MPA is characterized by increased proportions of cytotoxic CD8+ T cells, KIR+ CD8+ T cells, activated CD14+ monocytes, CD14+ monocytes with ISG expression, CD69+ naïve B cells, plasmablasts, and plasma cells. MPA was further subclassified into two groups based on the high expression of CD14+ monocytes signature genes (MPA-MONO) or high expression of ISGs (MPA-IFN). The percentage of monocytes and serum IFN-α levels were the clinical markers that clearly distinguished MPA-MONO and MPA-IFN groups, respectively. The findings of this study suggest clinical recommendations for estimating prognosis for each patient based on the immunological phenotypes of MPA. MPA microscopic polyangiitis, PBMC peripheral blood mononuclear cells, CITE-seq cellular indexing of transcriptomes and epitopes by sequencing, CyTOF cytometry by time-of-flight, CTL cytotoxic T lymphocytes, KIR killer immunoglobulin-like receptor, ISG interferon signature genes, MAIT mucosal associated invariant T cells, cDC classical dendritic cells, gdT gamma-delta T cells, CBC complete blood count.
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