Author: Ertugrul Cagri Bolek
Dürholz et al (POS0002) investigated proinflammatory effects of microbiota-derived mediators on synovial inflammation through metabolites such as short-chain fatty acids (SCFA) on mice model with collagen- or serum-induced arthritis. Their data show that the SCFA propionate effectively regulates ongoing inflammation by promoting histamine secretion of the gut microbiota and subsequent H3R-mediated neuronal effector functions that drive the fast resolution of synovial inflammation.
Singaraju et al (OP0015) explored that immune checkpoint inhibitor (ICI) arthritis enriched for CD38hiCD127– effector CD8+ T-cells compared to rheumatoid arthritis (RA) and psoriatic arthritis (PsA) and it is suggesting an elevated interferon signature. ICI therapies directly targets CD8 T-cells in patients with ICI-arthritis to trigger another autoimmune mechanism which is different from spontaneous autoimmune arthritis prototypes.
Izuka et al (OP0096) demonstrated immunophenotypic stratification of systemic immune-mediated diseases (systemic lupus erythematosus (SLE, n=78), mixed connective tissue disease (MCTD, n=22), idiopathic inflammatory myopathy (IIM, n=63), systemic sclerosis (SSc, n=52), RA, n=20, and large vessel vasculitis (LVV, n=19)) into 3 different clusters (C1, C2 and C3) according to predominance of naïve CD8+ T cells, memory CD4+ T cells, and non-classical monocytes, respectively. SLE was predominantly located in C2 and most of the SSc patients were in C3.
Horisberger et al (OP0186) performed immunophenotyping peripheral blood mononuclear cells (PBMC) from 140 patients with biopsy-proven SLE nephritis (LN) and 40 healthy controls using mass cytometry using four 48-marker panels. They identified potential and promising non-invasive biomarkers that altered naive B cell activation characterized as CD23– and CD21dim in proliferative LN and profoundly impaired circulating immunophenotype in LN patients.
Malmhäll-Bah et al (POS0239) explored transcriptome and RNAseq analysis on CD14+ and CD4+ cells of 77 TNF-inhibitors (TNFi) naïve active RA patients and 59 inactive RA patients treated with methotrexate (MTX, n=18), TNFi (n=10) and JAK-inhibitors (JAKi, n=24), or having no DMARD (n=7). The analysis suggested differentially expressed genes (DEG) with strong correlation to CDC42 defined the metabolic signature (MetSig) of CDC42hiCD14+ cells and they were antigen-presenting CD14+ cells migrating to joints and coordinating autoimmunity. JAKi can suppress the antigen presenting capacity of CD14+ cells and The MetSig in CD14+ cells may be useful to select candidate patients for JAKi.
Chirivi et al (OP0293) presented in vivo and vitro results of novel bivalent monoclonal antibody (CIT-013) with high affinity for citrullinated histones (H2A and H4) which targets neutrophil extracellular traps (NETs) pathway and reduces tissue NET burden. The data revealed that CIT-013 not only inhibits NETs release but also enhances phagocytosis and clearance of NETs.
ABOUT THE AUTHOR
Ertugrul Cagri Bolek
Ertugrul has recently completed his post-doc in Vasculitis Translational Research Program at National Institutes of Health (NIH).
He is currently focusing on translational research about vasculitides and rare rheumatic diseases in Turkey.
Ertugrul is the leader of the EMEUNET Country Liaison SubCommittee.