{
  "abstract": "Objectives Achieving durable remission in systemic lupus erythematosus (SLE) remains challenging and unpredictable due to clinical heterogeneity, fluctuating symptoms, and persistence of subclinical immune activation despite apparent clinical quiescence. Reliable biomarkers capable of identifying patients likely to sustain prolonged remission would enable more precise treatment tapering, reduce cumulative immunosuppression, and support personalised, remission-targeted management strategies. This study sought to investigate the immunological phenotype of patients with SLE in view of finding biomarkers associated with sustained disease remission.Methods We analysed serum samples of patients with SLE using the NUcleic acid Linked Immuno-Sandwich Assay (NULISA) Inflammation Panel 250 (Alamar). The assay uses a liquid biopsy platform for high-plex proteomic profiling of 250 inflammation markers, enabling target detection at attomolar sensitivity. Data were analysed after normalization and quality control. Thirty-four samples of patients diagnosed with SLE who were in clinical remission using both the BILAG and the SLEDAI scores at the time of their baseline visit divided into two groups; 1. Patients who developed at least one flare over a 5-year period post baseline (flare, n=11) and; 2. Patients who remained quiescent throughout (sustained remission, n = 23).Results The sustained remission group had significantly lower expression of 13 inflammatory markers compared with the flare group (p<0.05, figure 1). Sustained remission showed a broad dampening of innate/myeloid programs (lower IL12B, TREM2, GRN, and CSF3R), which indicates a downregulated IL-12/23 axis with reduced ‘danger’ sensing, and less granulopoiesis. Trafficking and vascular activation were also muted, with decreased CCL14, CCL23, CXCL16 and VEGFD consistent with reduced leukocyte recruitment and vascular remodelling. T cell maintenance and compensatory brakes subsided with lower IL7R, PD-L1 (CD274), and Galectin-9 (LGALS9), reflecting diminished demand for survival signals and inhibitory ligand induction. Finally, TNFRSF1B (TNFR2) was lower, implying less need for Treg/repair-linked TNF signalling. In contrast, flares re-engage these axes, producing the mirror pattern observed in those with sustained remission.Abstract PO:02:063 Figure 1Volcano plot showing differences in analytes between sustained remission and flareConclusions Deeper investigation using signature discovery and pathway analysis would help better understand the determinants of remission and risk of future flare in those who achieve remission in SLE. These pathways may also represent novel targets for future therapeutics.",
  "authors": [
    {
      "affiliations": [
        "Centre for Ageing, Rheumatology and Regenerative Medicine, London, UK"
      ],
      "name": "Rym Abida"
    },
    {
      "affiliations": [
        "National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, UK"
      ],
      "name": "Charis Pericleous"
    },
    {
      "affiliations": [
        "Centre for Ageing, Rheumatology and Regenerative Medicine, London, UK"
      ],
      "name": "Anisur Rahman"
    },
    {
      "affiliations": [
        "Department of Clinical and Academic Rheumatology King’s College Hospital, London, UK"
      ],
      "name": "Chris Wincup"
    }
  ],
  "title": "PO:02:063 The cytokine phenotype of sustained remission in systemic lupus erythematosus",
  "uid": "4a8eba03-8a31-5f4e-b5f4-a3845596a39e"
}