Dr Nikolaos Vlachogiannis
Country: Greece
Nikos is a postdoctoral researcher in Rheumatology and a resident in Internal Medicine at the Medical School of the National and Kapodistrian University of Athens. His clinical and research interests focus mainly on systemic sclerosis.
He serves as the EMEUNET Country Liaison for Greece and is a member of the EMEUNET Education Subcommittee. In addition, he is one of the Basic Science Group Coordinators for the EUSTAR Young Investigators.
| Oral 0888 | Sunday, 08.11.2026 09:30 Session: Abstracts: B Cell Biology & Targets in Autoimmune & Inflammatory Disease Presenting author: Carlo Tur (Germany) Title: Remodeling of the Cellular and Molecular Immune Landscape in Lymph Nodes Following CD19 CAR T-Cell Therapy  This study shows that CD19 CAR T-cell therapy induces immune remodeling in lymph nodes of patients with autoimmune diseases. Long-term follow-up revealed repopulation predominantly by naïve B cells, near-absence of memory B cells, and progressive plasma cell loss. Early regulatory T-cell expansion and redistribution across lymph node compartments was associated with enhanced immunoregulatory signaling. These findings suggest that CAR T-cell therapy establishes a new immunological homeostasis, potentially explaining sustained drug-free remission and supporting its role as an immune-resetting treatment. |
| Oral (Plenary) 0870 | Sunday, 08.11.2026 11:00 Session: Plenary I Presenting author: Aurélien Chepy (France) Title: Anti-Topoisomerase-1 Autoantibodies Exert Intranuclear Pathogenic Activity in Systemic Sclerosis Through FcRn-Dependent Trafficking This study shows that anti-topoisomerase-1 antibodies (ATA), detected in a subset of patients with systemic sclerosis (SSc), enter cell nuclei through neonatal Fc receptor (FcRn)-dependent trafficking, inhibit topoisomerase-1 activity, and induce DNA damage. This activates cGAS-STING signaling, promoting type I interferon responses and collagen production, thereby linking ATA directly to immune activation and fibrosis. FcRn blockade with efgartigimod prevented these effects in skin explants. These results demonstrate a direct pathogenic role for ATA in SSc. |
| Oral 0915 | Sunday, 08.11.2026 13:15 Session: Abstracts: Rheumatoid Arthritis – Translational Models and Mechanisms Presenting author: Jaeyeon Kim (USA) Title: Migration-dependent Synoviocyte-Endothelium Cross-talk in Rheumatoid Arthritis This study identifies a pathogenic interaction between fibroblast-like synoviocytes (FLS) and endothelial cells (ECs) in rheumatoid arthritis (RA). FLS actively migrate across synovial capillary walls, a process associated with disease activity. FLS migration was dependent on polycystin-1 (PKD1) and induced endothelial cathepsin K (CTSK) expression, promoting angiogenesis and vascular permeability. Experimental PKD1 inhibition reduced FLS migration and arthritis severity. These findings reveal a strong interplay between FLS and ECs promoting synovial inflammation in RA. |
| Oral 1850| Monday, 09.11.2026 08:00 Session: Abstracts: Spondyloarthritis Including Psoriatic Arthritis – Basic and Translational Science Presenting author: Isabel Risch (USA) Title: Defining A Signature of Autoreactive CD8+ T Cells in HLA-B27-Associated Autoimmune Disease This study identifies a conserved transcriptional and functional signature of autoreactive CD8+ T cells across HLA-B27-associated inflammatory diseases. These cells exhibit a distinct type 17-like phenotype, characterized by IL-17A and IL-22 production, and share transcriptional features across blood, intestine, inflamed joints, and eyes. Detection of autoreactive T-cell receptors in intestinal samples suggests that their pathogenic differentiation may originate in the gut. These findings support a common immunological mechanism underlying HLA-B27-associated diseases. |
| Oral 1821| Monday, 09.11.2026 10:15 Session: Plenary II Presenting author: Benjamin Jones (USA) Title: Molecular Heterogeneity in Preclinical Lupus: Distinct Longitudinal Proteomic Trajectories Preceding Disease Progression. This study identifies three distinct soluble proteomic trajectories among individuals with incomplete lupus: Group 1 showed increasing interferon-immune responses associated with systemic/hematologic progression. Group 2 showed downregulation of innate immune signaling associated mainly with articular/mucocutaneous progression. Group 3 displayed relatively stable immune profiles and predominantly cutaneous progression. These results suggest that baseline proteomic profiling could improve risk stratification and guide personalized SLE prevention strategies. |
| Oral 1904| Monday, 09.11.2026 15:00 Session: Abstracts: Systemic Lupus Erythematosus – Etiology & Pathogenesis Presenting author: Rayan Najjar (USA) Title: Neoantigens Recognized by B and T Cells are Generated by Aberrant mRNA Splicing in Lupus Neutrophils This study identifies aberrant mRNA splicing in neutrophils of lupus patients. Researchers detected 271 lupus-specific cryptic splicing events across 130 protein-coding genes, including many interferon-stimulated genes. Experimental validation confirmed their translation and binding to MHC-I, and demonstrated both IgG antibody responses and antigen-specific T-cell activation against these cryptic peptides. The abnormalities were enriched in neutrophils and were not reproduced by type I interferon stimulation. These findings reveal cryptic splicing-derived neoantigens as potential drivers of immune activation in lupus. |